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Flashcards in Microbiology: Fungi Deck (18):

Difference btwn fungi and bacteria

-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


Reproduction of fungi

-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)


Types of conidiospores

-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)


Classification of fungi

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


Classification by tissue involvement

-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


Classification by host response (primary vs. opportunistic)

-Opportunistic: candida (endogenous flora), aspergilla and cryptococcosis (exogenous)
-Primary: Blastomycosis, histoplasmosis, coccidiomycosis (and paracoccidiodomycosis), penecilliosis (all exogenous)


Immune response to fungi

-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


Immunocompromised hosts

-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


Ways to Dx fungal infections

-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


Problems w/ fungal testing

-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)


Targets of anti fungal drugs

-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)


Coccidiodes Immitis

-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)


Coccidiodes pathogenesis

-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


Candida Albicans

-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)


Candida pathogenesis

-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


Aspergillus Sp.

-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)


Aspergillus pathogenesis

-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


Important immune responses to fungal infection

-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