Microbiology: Fungi Flashcards

1
Q

Difference btwn fungi and bacteria

A
  • Fungi are eukaryotic, bacteria are prokaryotic
  • Also have cell wall, but it is made up of complex polysaccharides (chitin, B-glucan)
  • Fungal cell membranes are composed of ergosterol
  • Fungi can be dimorphic (only primary fungi), often depending on temperature (thermodimorphic)
  • Switch from mold form (@ 25 C: grow via hyphae, multicellular filamentous form w/ apical extension) to yeast form (@ 37 C: grow via budding or fission to make round unicellular colonies)
  • Aspergillus is mold only fungi, and candida is yeast only fungi
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2
Q

Reproduction of fungi

A
  • Can reproduce sexually or asexually
  • Asexual spores can be sporangiospores, which are contained in the sporangium, or conidospores, which are borne naked on specialized structures called conidia
  • Most medically important fungi reproduce asexually
  • Once spores find suitable habitat they germinate into germ tube (initial hypha)
  • Germ tube grows into larger hypha (vegetative), and eventually sprouts stalks (aerial hypha) to bear conidia and conidiospores
  • Hypha are either septate (divided by partitions in cell wall) or non-septate (hollow and multinucleate)
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3
Q

Types of conidiospores

A
  • Spores are always formed from fruiting (aerial) hypha
  • Arthrospores are spores that are formed by fragmentation (every other cell dies)
  • Blastospores: very small round cells in clusters, formed by budding
  • Chlamydospores: larger round cells w/ thicker walls (formed in unfavorable conditions)
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4
Q

Classification of fungi

A
  • Formal taxonomy
  • By reproductive cycle (sexual/asexual spores)
  • Degree of tissue involvement
  • By host response (primary or opportunistic)
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5
Q

Classification by tissue involvement

A

-Superficial infections: growth restricted to stratum corneum of skin
-Cutaneous fungal infections (dermatophytes): keratinophilic and more invasive than superficial mycoses, but still limited to keratinized tissue
-Mucocutaneous infections: mucous membranes
Subcutaneous infections: subcutaneous tissue due to trauma
-Systemic infections (primary fungi): inhalation or tissue trauma, mostly affects lung or skin, subsequent dissemination is possible
-Systemic infections usually caused by dimorphic (primary) pathogens that are endemic to regions

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6
Q

Classification by host response (primary vs. opportunistic)

A
  • Opportunistic: candida (endogenous flora), aspergilla and cryptococcosis (exogenous)
  • Primary: Blastomycosis, histoplasmosis, coccidiomycosis (and paracoccidiodomycosis), penecilliosis (all exogenous)
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7
Q

Immune response to fungi

A
  • Cell-mediated immunity more important than humoral immunity
  • PMNs, macrophages, T cells are all involved in eliminating the infection (phagocytes recognize PAMPs on fungi; pathogen-associated molecular patterns)
  • Of the T cells mostly Th1 is involved
  • Abs do have role (but not neutralizing except for toxins): prevention of adherence, opsonization, neutralization of toxins
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8
Q

Immunocompromised hosts

A
  • Most patients of fungal infections are IC’d (often infected w/ opportunistic fungi)
  • Includes: patients w/ long antibio Rx, those on immunosuppressive drugs (transplants, autoimmune), radiation/chemo therapy, diabetes (endocrine disorders), AIDS (congenital or acquired immunodeficiencies), malnutrition, low birthweight neonates
  • Also: AGED
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9
Q

Ways to Dx fungal infections

A
  • Direct microscopic examination from biopsy (opportunistic can be hard to interpret)
  • Culturing and determination through morphological and biochemical criteria (may require weeks b/c primary fungi grow slowly)
  • Serology: detect Ab’s in serum (cannot tell if positive test means current or prior infection), skin test (DTH) to measure exposure to fungal Ags (testing cell-mediated immunity)
  • Can also detect disseminated Ags in blood, or via DNA probes
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10
Q

Problems w/ fungal testing

A
  • IC’d patients may lack Ab response
  • Some opportunistic fungi do not produce Ab response
  • DTH response may not occur due to anergic T cells (in IC’d patients)
  • Positive DTH test does not distinguish which species (can cross react)
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11
Q

Targets of anti fungal drugs

A
  • Polyenes: target ergosterol on cell membrane (amphotericin B)
  • Azoles: interfere w/ ergosterol synthesis (interrupt cell and mitochondrial membrane synthesis)
  • Echinocandins: inhibit B-glucan synthesis in cell wall
  • Nucleoside analogs: inhibit DNA/RNA synthesis (5-fluorocytosine)
  • Grisefulvin: binds to microtubule associated proteins and prevents spindle formation at metaphase (targets keratin, for cutaneous infections)
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12
Q

Coccidiodes Immitis

A
  • A primary fungi that is endemic (to southwest US) and shows thermodimorphism (can infect immune competent host), found in soil
  • Forms infectious arthrospores (infects via inhalation)
  • Arthrospores swell and develop into spherules filled w/ endospores. Each endospore develops into new spherule
  • Arthrospores have antiphagocytic activity, spherules are too large to phagocytose
  • Elicits both PMN and CMI (cell-mediated immunity) response (mostly Th1)
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13
Q

Coccidiodes pathogenesis

A
  • Causes coccidiodomycosis
  • Inhalation of athrospores causes pulmonary infection (most are asymptomatic)
  • 40% have mild-severe symptoms (usually IC’d)
  • 5% lead to dissemination (to skin, soft tissue abscesses, bone and joints, meningitis)
  • Dx: flu-like symptoms, microscopy of spherules, culture (25C and 37C for both forms), serology (blood Abs, CSF Abs, DTH test)
  • Rx: Amphotericin B, itraconazol, fluconazole
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14
Q

Candida Albicans

A
  • Opportunistic fungi of normal flora, often infects patients undergoing antibio therapy, neutropenic, and also AIDS/HIV patients
  • Produces pseudohypha (NOT MOLDS), in filamentous form it has better survival against host defenses (phenotype switching)
  • Usually lives in yeast form, replicates via budding
  • Normally lives in URT, GIT, FGT (female genital tract)
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15
Q

Candida pathogenesis

A
  • Causes candidosis
  • Non-systemic infections: mucocutaneous (ileum, esophagus, vaginitis, thrush), cutaneous (dermatitis, keratinitis)
  • Systemic: UTI, ednocarditis, meningitis, sepsis
  • Dx: microscopy (budding yeast and/or pseudohypha), culture (germ tube test, specimens from blood, sputum, urine), sugar assimilation panel
  • Rx: Amphotericin B, fluconazole, caspofungin, 5-flucytosine
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16
Q

Aspergillus Sp.

A
  • Exogenous opportunistic (ubiquitous), do not exhibit dimorphism (ONLY MOLD FORM)
  • Mostly infects IC’d patients, usually neutropenic
  • Inhalation is point of entry
  • Cell wall components aid in adherence to host proteins
  • Posses cell wall pigments (melanin) that interfere w/ phagocytosis
  • Toxins and extracellular nzs that lead to hemorrhage/necrosis/invasion (angioinvasive)
  • Poor prognosis for patients on corticosteroids (IC’d)
17
Q

Aspergillus pathogenesis

A
  • Causes aspergillosis: infection of lung-> invasion of blood vessels-> spread to brain, kidney, liver, heart, bone
  • Dx: Suspicion should provoke anti fungal therapy, then run tests. Chest Xray will reveal lung infection (aspergilloma, fungus ball), CT scan of other organs. Microscopy shows Y shaped filaments (use sputum), Ag (galactomannan from cell wall) and IgE Ab detection
  • Rx: Amphotericin B, caspofungin, removal of fungus ball
18
Q

Important immune responses to fungal infection

A
  • CMI is most important, particularly Th1 response, but also macrophages, PMNs, dendritic cells
  • Th1 are primary cells for resolving infections, Th2 help neutralize/control infection
  • Yeast forms are easier to handle b/c they elicit a larger Th1 response and a smaller Th2 response
  • Conversely, hypha forms are more difficult to eliminate b/c they elicit a smaller Th1 response and a larger Th2 response