Beginning Fungi

Front 1

What are the 2 forms that a single dimorphic Fungi can live in? What is the major difference between these?

Back 1

Yeast - unicellular (smooth individual colony)
Molds - multicellular (entangled filamentous)

Front 2

What are some gen characteristics of fungi?

Back 2

Rigid cell wall (glucan and chitin)
Haploid
No chlorophyll

Front 3

How do yeast reproduce?

Back 3

through budding

Front 4

What are pseudohyphae?

Back 4

These are long chains of cells formed from yeast that bud but remained attached. the cytoplasma are NOT connected. This is different from septated hyphae.

Front 5

What are the 2 types of molds?

Back 5

Septated hyphae
and
Non septated hyphae *typical of zygomycetes"

Front 6

What differentiates the 2 types of molds?

Back 6

septated hyphae - have membranes that separate each cell
&
non septated - lack the dividing membranes and thus are multinucleated cells

Front 7

What does a dimporhic mold refer to?

Back 7

Its ability to live in 2 different forms.
-
Often they are temperature dependent

Front 8

What are unique substances in fungi walls?

Back 8

ergosterol and chitin

Front 9

How are the cell wall properties effect the ability of antibiotics to work on fungi?

Back 9

Antibiotics are often not functional against fungi
- No peptidoglycans (chitin instead)
&
Antifungals target
-Ergosterol ect

Front 10

What are mechanisms of antifungals?

Back 10

They target ergosterol
- Ketaconazole = inhibit ergosterol synthesis
- Amphoteracin B = pore forming at site of ergosterol
- Nystatin = pore forming at site of ergosterol (topical including GI topical)

Front 11

How can fungal infections be categorized?

Back 11

Based on how they infect and where

Front 12

What are the fungal categories? (4)

Back 12

Cutaneous
Subcutaneous
Systemic
Oppurtunistic

Front 13

Major function Fungi in nature and how relate to metabolism?

Back 13

NO chloroplasts
Decomposers as carbon source
+
Nitrate/NH3 as Nitrogen source

Front 14

What type of patients typically get mycoses?

Back 14

immunocompromised

Front 15

What type of infections are typically caused by fungi

Back 15

mycoses vary greatly in their manifestations but tend to be subacute to chronic with indolent, relapsing features.
-
acute diseasae is rare

Front 16

What is organization of fungi?

Back 16

A yeast cell showing the cell wall and internal structures of the fungal eukaryotic cell plan
-
The rigid cell wall external to cytoplasmic membrane has a different composition

Front 17

What are the differences in membrane sterol compositions between fungi and humans?

Back 17

Fungi - ergosterol
Humans - cholesterol

Front 18

What is the significance of fungi having eukaryotic organization?

Back 18

More of the structures are similar to human cells and HARDER to differentiate from non pathogenic, self cells

Front 19

What is the composition of fungal cell walls?

Back 19

Mannan, glucan, & chitin
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The fungal cell wall. The overlapping mannan, glucan, chitin, and protein elements are shown. Proteins complexed with the mannan (mannoproteins) extend beyond the cell wall.

Front 20

What bactrerial structures are fungi missing that are found in bacteria?

Back 20

Different in that bacterial cells in that it does not contain peptidoglycan, glycerol or ribitol teichoic acids, or lipopolysaccharide

Front 21

Gram-positive envelope.

Back 21

Major components of Gram-positive walls are peptidoglycan and teichoic acid
--
Peptidoglycan comprises glycan chains cross-linked by peptide chains

Front 22

Gram-negative envelope.

Back 22

Gram-negative outer membrane is phospholipoprotein bilayer, of which the outer leaflet is LPS endotoxin

Front 23

What are the major determinants of serological specificty in fungi?

Back 23

Mannoproteins are mannose-based polymers (mannan) found on the surface and in the structural matrix of the cell wall, where they are linked to protein.

Front 24

Chitin function in yeast v. mold

Back 24

In filamentous mold - form the wall that is insulble, rigid, and inert
-
In yeast - forms cross septa & channels so nuclei can pass to progeny

Front 25

What is the difference in function betw/ Glucans and mannans?

Back 25

Glucans - w/ chitin give rigidity to cell wall
-
mannan is on surface and gives serological differences

Front 26

Are fungi aerobeic or anaerobic?

Back 26

All that cause disease in humans are strict aerobes.

Front 27

What are conidia? What methods are they produced by?

Back 27

These are the reproductive elements in asexual (anamorphs). Haploid under go mitosis
-
Produced by budding, fragmentation, or sporulation. (iamge)

Front 28

What are spores? Haploid or diploid?

Back 28

These are reproductive structures in the sexual (telomorph)
Haploid combine to become diploid and divide by meosis

Front 29

What are the mechanisms in asexual and sexual reproduction? What are the products?

Back 29

Asexual reproduction forms conidia by mitosis
-
Meiosis forms sexual spores in specialized structures

Front 30

What are Blastoconidia and conidophores?

Back 30

Yeast and mold forms of fungal growth. A. This oval yeast cell is budding to form a blastoconidium. Scars from the separation of other blastoconidia can be seen on other parts of the cell. B. The mold form is highly variable. Here tubular stalks called condiophores arising from hyphae (not seen) bear a "Medusa head" crop of reproductive conidia

Front 31

Describe the structure of septated/nonseptated hyphae & pores that join these structures

Back 31

Hyphae. A. Nonseptate hyphae with multiple nuclei. B. Septate hyphae divide nuclei into separate cells. C. Electron micrograph of septum with a single pore. D. Multipore septum structure.

Front 32

What is the fluffy portion of mold? How else may they grow?

Back 32

The more visible surface growth may assume a fluffy character as the mycelium becomes aerial.
Hypahe may grow along, into or above the substrate

Front 33

What is the function of the fluffy component of mold?

Back 33

The aerial hyphae bear the reproductive structures of this class of fungi.

Front 34

What is the importance of conidia?

Back 34

Morphology of reproductive conidia and spores used for identification

Front 35

What are the different conidia and what defines them?

Back 35

(CASS)
-------------------------------
Asexual mold forms. A. Arthroconidia develop within the hyphae and eventually break off. B. Chlamydoconidia are larger than the hyphae and develop with the cell or terminally. C. Sporangiocondia are borne terminally in a sporangium sac. D. Simple conidia arise directly from a conidiophore

Front 36

What stages are typical in a temperature dimorphic fungi?

Back 36

Yeast phase growth requires conditions similar to those of the physiologic in vivo environment, such as 35° to 37°C incubation and enriched medium. Mold growth requires minimal nutrients and ambient temperatures.

Front 37

Do we typically see molds in humans? Why and give example?

Back 37

No, due to the host temperature that promotes yeast
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Histoplasma capsulatum. They are understandably complex, given the dramatic change of milieu encountered by the fungus when its mold conidia float from their soil habitat to the pulmonary alveoli. Conversion to the yeast phase is then triggered by the host temperature (37°C) and possibly by other aspects of the new environment.

Front 38

Is dimorphism reversible?

Back 38

yes, this is why it is not considered a embryogenesis type proceess

Front 39

What is unique about the medically releavnt fungi? How does this effect classification? (NEED TO SHORTEN ANS)

Back 39

A major issue in classifying the medically important fungi using these groups is that for most species, no teleomorph form has been demonstrated. It may be that because of an advantage for pathogenicity, persistently anamorph clones were selected during evolution, or that the conditions for natural production of spores are just yet to be met.

Front 40

What do we do about the difficulty in classifying fungi? So then what do we do about it?

Back 40

we make up artificial groups
-
types of tissues they parasitize and the diseases they produce, rather than on the principles of basic mycologic taxonomy.

Front 41

What about Superficial fungi?
-Name?
-Common examples?

Back 41

superficial fungi, such as the dermatophytes, cause indolent lesions of the skin and its appendages, commonly known as ringworm and athlete's foot.

Front 42

What about subcutaneous fungi?
-Where do these typically spread to?

Back 42

subcutaneous pathogens characteristically cause infection through the skin, followed by subcutaneous spread, lymphatic spread, or both.

Front 43

What about opportunistic fungi?
-where do these reside?
-type of host?

Back 43

The opportunistic fungi are those found in the environment or in the normal flora that produce disease under certain circumstances and in the compromised host.

Front 44

What about systemic fungi?
-comparative virulence?
-type of host?

Back 44

The systemic pathogens are the most virulent fungi and may cause serious progressive systemic disease in previously healthy persons. They are not found in the normal human flora.

Front 45

Why is KOH used in fungal preps?

Back 45

KOH digests tissue, but not fungal wall

Front 46

Describe how and what ringworm could be diagnosed?

Back 46

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KOH (potassium hydroxide) preparation. Scalp scrapings from a suspected ringworm lesion have been mixed with 10% KOH and viewed under low power. The skin has been dissolved, revealing tubular branching hyphae.`

Front 47

How are fungi visualized?

Back 47

fungi can be observed under the light microscope with or without staining

Front 48

How are fungi cultured?

Back 48

They grow slowly
Grow under normal condition but bacteria outpace the
Selective media make use of antimicrobics
Typically grow @ 30c

Front 49

What are hyphae?

Back 49

Each of the branching filaments that make up the mycelium of a fungus. May be septated or not. Growth occurs at the tip

Front 50

What are mycelium?

Back 50

Sun of the hyphae. The vegetative part of a fungus, consisting of a network of fine filaments (hyphae)

Front 51

(Bactrerial) What is the difference betw/ lipotechoic acid and techoic acid?

Back 51

lipotechoic acid has lipid that allows it to associate with the inner cell membrane. Techoic acid does not have the ability to associate w/ lipid bilaye

Front 52

Are fungi in flora?

Back 52

yes, these might be the opportunistic classified fungi
Primarily thing Candida Albicans. Candida is indigenous to GI tract

Front 53

What type of pathogenesis (general) that fungi cause?

Back 53

----------------------
Fungi system view. Localized disease (left) is produced by local trauma or the superficial invasion of flora resident on the oropharyngeal (thrush), gastrointestinal, or vaginal mucosa. Systemic disease (right) begins with inhalation of conidia followed by dissemination to other sites.

Front 54

What is the immunological response to Fungi?

Back 54

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Immunity to fungal infections. A. Pathogenic fungi are able to survive and multiply slowly in non-activated macrophages. B. When macrophages are activated by cytokines from T-cells the growth is restricted and the fungi digested.

Front 55

What are the majority of pathogenic fungi? What are some examples?

Back 55

Oppurtunistic
Examples - Aspergillus, Zygomycetes, Pneumocystis

Front 56

What is the ability to adhere associated with in fungi?

Back 56

Virulence

Front 57

How do fungi adhere?

Back 57

Adherence usually requires a surface adhesin (mannoprotein) on the microbe and a receptor on the epithelial cell. (fibronectin)
I.e. Candida Albicans - mannoprotein (common in many)

Front 58

What is a virulence factor in fungi that infect lungs?

Back 58

Small so they are suspended in air and reach terminal bronchioles

Front 59

What is invasion by fungi associated with?

Back 59

It is associated with enzymes secrete from tip of hyphae.
-----------------
Extracellular enzymes (eg, proteases, elastases) are associated with the advancing edge of the hyphal form of Candida and with the invasive forms of many of the dimorphic and other pathogenic fungi. Although these enzymes must contribute to some aspect of invasion or spread,

Front 60

Do fungi have exotoxins? Then what causes necrosis and infarction?

Back 60

No, it has not been oberved in vivo
----------
presence of necrosis and infarction in the tissues of patients with invasion by fungi such as Aspergillus suggests a toxic effect, direct evidence is lacking.

Front 61

What causes most of the injury in fungal infections?

Back 61

The injury caused by fungal infections seems to be due primarily to the destructive aspects of delayed-type hypersensitivity (DTH) responses as a result of the inability of the immune system to clear the fungus. >

Front 62

What type of infection do fungal parralel

Back 62

In this respect, fungal infections resemble tuberculosis more than any other disease

Front 63

What is the role of innate immunity to fungi?

Back 63

High level, which is why most fungi are oppurtunistic

Front 64

What innate immune mechanisms are antifungal?

Back 64

1. professional phagocytes (neutrophils, macrophages, and dendritic cells)
2. complement system
3. pattern recognition receptors - lectin like (binds glucan)

Front 65

What mediates the the resolution of fungal infection?

Back 65

In most instances in which it has been investigated, the actions of neutrophils and TH1-mediated immune responses have been found to be of primary importance in this resolution. (T cell mediated response)

Front 66

What is the role of adaptive humoral immunity to fungal infections?

Back 66

Most fungal infections will have some Ab formation but response is dominated by CMI
-Cryptococcous neoformans = Ab help
-Coccidioidomycosis Imitus = Ab bad (dissemination/worsening)

Front 67

What type of pts get severe systemic fungal infections?

Back 67

Systemic neutropenia or depressed Th1 (T cell) repsonses

Front 68

How do some fungi escape PMNs?

Back 68

Fungi that escape neutrophils grow slowly in macrophages

Front 69

What are the steps of cellular response to fungi and what effect do they have?

Back 69

Fungi
Interaction DC & macrophages favors production IL4 & IFNgamma -> CD4 become Th2 cells -> activate B cells to secrete neutralizing Ab (killing) [extracellular microbes]
***Turning point when host fight fungal infection***
Th1 response - T cells activate macrophages via IFNgamma & . Now macrophages are able to restrict intracellular growth of fungi. Any secreted Ab are for opsonizing pathogens

Front 70

What is the important mechanism to attack fungi?

Back 70

The CMI or Th1 response that is depndent on macrophages and their activation

Front 71

What are the sexual fruiting bodies?

Back 71

Top - zygospore (yoke)
Mid - Ascospore (sac)
Bot - basidiospore (club)

Front 72

How are glucans used by medical personelle?

Back 72

Measure circulating levels Beta glucan to detect invasive systemic fungi
Glucan Synthetase inhibitors - antifungals

Front 73

Summary medical fungi

Back 73

Front 74

What are the endemic fungi?

Back 74

Blastomycetes
Coccidioides
Cryptococcus
Histoplasma

Front 75

What are the targets for antifungals? (7)

Back 75

Front 76

What are the 7 antifungal classes?

Back 76

Flucytosine
Terbinafine
Azoles
Amphoteracin B
Echinocandins
Nikkomycin Z
Griseofulvin