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Medical Biochemistry and Pathophysiology > Week 7A: Medical Yeasts, Virulence, Antifungals, Brain metabolism > Flashcards

Week 7A: Medical Yeasts, Virulence, Antifungals, Brain metabolism Flashcards

HC 37, 38, 39

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USMLE® Step 1 flashcards
1
Q

Tinea capitis

A

Trinchophyton schoenleinii (fungus) grows in hair follicles > bald head
> Scalp ringworm
> hair contains protein: carbons hydrogen and sulfur as nutrients

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2
Q

Tinea Circinate

A

Ringworm causes ring inflammed round scaly lesion lower on body (chest)

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3
Q

Tinea pedis

A

Zwemmerseczeem, between toes

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4
Q

Onychomycosis

A

Infection of nails by fungi

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5
Q

Risk treating fungi

A

If one cel survives, it can grow back

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6
Q

Candidas are easier treatable when they are … and not …

A

superficial and not invading the system

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7
Q

Mycoses meaning

A

Diseases caused by fungal infection

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8
Q

Pathogenic fungi vs opportunistic fungi

A

Pathogenic
> cause disease in both immunocompetent and immunocompromised hosts
Opportunistic
> cause disease in immunocompromised hosts
> immune resistance of host compromised
> can cause life threatening disease

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9
Q

Immunocompromised host

A

Immunity is altered, because
-Presence debilitating disease, like AIDS
-Immunosuppressive drugs

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10
Q

Name the three opportunistic fungi we need to know for the course and their fungal groups

A

Candida albicans > Hemiascomycetes
Aspergillus fumigatus > euascomycetes
Cryptococcus neoformans > basidiomycetes

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11
Q

Difference ascomycetes and basidiomycetes in secual cycle

A

During sporulation, ascomycetes form an ascus (sac), and basidomycetes form a basidium (mushroom like)

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12
Q

Ascospore formation

A

> Haploid + and - cells fuse to diploid
Diploid cell
meiosis
Four nuclei in one PM
ascospore formation
Four spores in one membrane sac (ascus)
autolysis
Ascospores (seperate)

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13
Q

Aspergillus fumigatus asexual spores

A

Condidia
> Vescicle with a lot of tubes which bud of conidia (ev conidium)
> release A LOT of spores
> conidia are the tiny spores that go into the air from the vesicle.

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14
Q

Hemiascomycetes type

A

budding yeast like fungi and candida albicans

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15
Q

Aspergillus fumigatus characteristic of infection

A

Fall on food and grow
> euascomycete

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16
Q

Reproduction aspergillus fumigatus

A

Sexually (ascospores) and asecual (conidia)

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17
Q

Organ transplantation is a danger for..

A

fungus infection if spores there

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18
Q

Invasive aspergillosis has a … mortality rate

A

high
> especially in liver, bone marrow of brain

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19
Q

Candida albicans form …. on blood plates

A

white colonies
> blood is rich in nutrients for fungal growth
> cryptococcus not white: attracts water

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20
Q

Morphological switch in Candida albicans

A

Can switch reversibly between yeast form and hyphal form
> hyphal form has directional growth (like tubes of cells)
> fully reversible and essential for virulence
> triggered by conditions

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21
Q

Yeast-to-hypha transition in candida albicans

A

Yeast cells form germ tubes which grow out

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22
Q

What kind of fungus is C albicans and how where does it reside?

A

Opportunistic yeast
> commensal life on skin and mucose of GI tract > occupy spaces so that nasty microorganisms cannot grow there

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23
Q

Invasive systemic infection of C. albicans in patients with …, and which organs affected make it life threatening

A

compromised immune system
> life threatening: infections of liver, kidneys and brain.

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24
Q

Candidiasis

A

Infection caused by Candida species

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25
Q

Superficial candidiasis

A

Local infection

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26
Q

Hyphal C.albicans can penetrate …

A

the epithelium > invasion > switch back to yeast form which can travel through blood
> immune cells do not attack when immunocompromised

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27
Q

Why do males and females with T2DM have risk for Candida infection at penis head or vagina?

A

Glucose in the urine > nutrients
> candida balanitis

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28
Q

Risk factors Candida albicans infection

A

-T2DM
-(broad spectrum) antibiotics (less competition for fungus, normally all the niches are occupied by bacteria)
-Immune suppressants
-Catheters
-Prosthetic devices
-Abdominal surgery
-Needle: push it into blood

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29
Q

Phagocytosis Candida in vitro by macrophages

A

After a while the germ tube is formed (morphological switch) aand hyphal penetrates the cell and kills it
> a lot of building blocks in the lysosomes of the macrophages to make fungi grow

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30
Q

Defensive reaction macrophages upon phagocytosis candida

A

Oxidative stress > respiratory burst
> produce ROS to attack Candida

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31
Q

Triggers of morphological switch in Candida

A

-Absence nitrogen and carbon: poor conditions
-pH, serums and ingestion by macrophages
> sensing proteins and TFs involved: programs for hyphal form activated

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32
Q

Why is the morphological switch of C. albicans a virulence factor

A

Otherwise it cannot kill the macrophages by switching to hyphal form

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33
Q

Candida auris

A

An emerging fungus
> invasive and picked up in the hospital
> treatable with echinocandins
> some strains are multidrug resistant
> hospital-acquired infection

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34
Q

Cryptococcus neoformans defensive structure

A

Capsule
-Hair like molecules around them (around the PM
> harder to take up by phagocytes

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35
Q

The cell compartments of the fungus makes it clear why it is hard to make fungal drugs,: explain

A

It resembles the human cell
> neokaryotes: make new nucleus
> eukaryote
> contain peroxisomes (vacuoles in fungi and yeast), lysosomes, ER, mitochondria
> drug should not kill human cells

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36
Q

Melanin in cryptococcus neoformans

A

Protect cells against oxidative burst inside immune cells
> the ROS of macrophages and neutrophils cannot penetrate it
> in multiple fungi present: virulence factor

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37
Q

Virulence factors

A

Molecules expressed by pathogenic and opportunistic organisms that are important to cause disease in the host
> can be lipids, carbohydrates, proteins
> ideal target for antifungal drugs

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38
Q

Factors that are involved in basic cellular metabolism are essential for survival of a microorganism in the host, but they are not called virulence factors. Why?

A

They do not influence the host directly

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39
Q

Why does Cryptococcus neoformans appear glazy on blood plate

A

Carbohydrate (polysaccharide) capsule
> attracts water

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40
Q

How does Cryptococcus neoformans synthesize melanin: which precursor

A

From L-DOPA (dopamine precursor)

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41
Q

Melanin production enzyme and reaction of committed step

A

L-DOPA > Dopa quinone (enzyme: laccase, phenoloxidase involved in melanin formation)

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42
Q

Laccase

A

Phenoloxidase involved in formation of melanin

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43
Q

Melanin in cryptococcus neoformans protects against:

A

-Environmental stresses such as ionizing radiation
-Oxidative damage by phagocytes

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44
Q

Melanogenesis in Cryptococcus

A

-L-DOPA > Dopa quinone (laccase/ phenol oxidase)
-Spontaneous autooxidation steps from Dopa quinone to melanin

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45
Q

Two virulence factors Cryptococcus neoformans

A

-Melanin
-Capsule

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46
Q

Capsule cryptococcus neoformans

A

High molecular weight polysaccharide: Glycuronoxylomannan (GXM)
> major repeat unit + serotype

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47
Q

Cryptococcus survival inside macrophages

A
  1. Phagocytic uptake
  2. Phagolysosome formation
  3. late stage trafficking markers
  4. rupture phagosomal membrane
    > love acidic environment and secrete lipases to break down lysosome > slow digestion macrophage contents for nutrients due to not optimal pH)
  5. growth Cryptococcus in cytosol
  6. rupture hos cell > releasing cell after 8-18h after ingestion
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48
Q

Mode of action of defense of macrophages and neutrophils

A

Oxygen-independent mechanism
> Hydrolytic enzymes: proteases and lipases
> Defensins: microbicidal peptides
> nutrient deprivation
Oxygen-dependent mechanism
> ROS and nitrogen species: O2-‘, H2O2, NO’
> HOCl (hypochlorite, only in neutrophils because they have the enzyme)

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49
Q

Identification and testing virulence factors

A

-Identification
-Gene deletion: KO
-Virulence assays with deletion strain and control (in vitro and in vivo)
-Virulence factor > target for antifungal drug design

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50
Q

Capsule assay cryptococcus as virulence factor: which samples included

A

-Wild type
-Cap10 mutant (acapsular mutant)
-cap10 mutant transformed with empty vector
-cap10 mutant transformed with cap10 gene
> survival when cap10 mutant or cap10 mutant with empty vector, and quickest death when transformed with cap10 vector: many copies of the gene > more of the limiting virulence factor

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51
Q

How are Aspergillus fumigatus, Candida albicans and Cryptococcus neoformans acquired>

A

-Aspergillus fumigatus: in air
-Candida albican: commensal in GI tract
-Cryptococcus neoformans: in GI tract of birds > bird poop air breathed in when walked over.
> gobbled up by alveolar macrophages

52
Q

HC38: Manganese, iron and zinc are …

A

Transition metal

53
Q

Transition metals are involved in which reactions in biochemistry?

A

One-electron reduction or oxidation reactions
> can deal with individual electrons

54
Q

Coordinate bonds in insulin hexamer

A

Two Zinc ions coordinated each by three His residues
> problem when mutated

55
Q

Binding manganese cofactor in managese superoxide dismutase

A

Bound by three Histidine side chains and one aspartate side chain
> water molecule and the inhibitor azide can be coordinated by manganese

56
Q

Stucture of the antifungal polyene called amphotericin B

A

ring with two large carbon chains. One has many hydroxyl groups and is hydrophilic. The other has many di-een groups (double bonds) and is hydrophobic)

57
Q

Function amphotericin B and other polyenes

A

Bind to sterols
> ergosterol in fungi > in PM
> adheres with hydrophobic side: make hydrogen bonds with carboxylic acid group between hydrophobic and hydrophilic chains (this groups faces towards the hydrophilic head of the phospholipids which lay next to the ergosterol which binds with its hydrophilic OH group to the polyene
> two rings of 8 molecules form hydrophilic channel when hydrophilic chains face eachother
> Pore: content flows out (leakage Mg2+ and K+ and others), cell dies

58
Q

Polyenes are fungi….

A

Fungicidal: the fungus is killed

59
Q

How does ergosterol differentiate from cholesterol

A

Extra double bonds

60
Q

Structure azoles

A

Ring of carbons with a nitrogen in it
> heterocycles of carbon and nitrogen atoms

61
Q

A diazole is characterized by?

A

Two nitrogens in the heterocycle

62
Q

Miconazole is a … and fluconazole is a …

A

Diazole, triazole

63
Q

Azoles are fungi….

A

Fungistatic
> Inhibits growth of fungi
> If the patients stop taking azoles, the fungi will grow again
> take for rest of life

64
Q

Azoles can bind …

A

The heme group with the transition metal iron

65
Q

CYP51 in fungi is involved in…

A

Ergosterol production from lanosterol
> Lanosterol 14a-methyl demethylation
> and then for two other methyl groups

66
Q

Azoles are inhibitors of …

A

Fungal CYP51

67
Q

Mechanism of action Voriconazole and Posaconazole

A

Voriconazle binds in binding pocket where lanosterol binds with the O2 (at the iron metal)
Posaconazole binds in a different binding groove and then also to the heme group. > stronger interaction

68
Q

How many oxygens needed to remove one methyl group?

A

Three molecular oxygens (O2)

69
Q

Function terbinafine

A

Block the conversion of Squalene to Squalene-2,3-epoxide in the synthesis of ergosterol
> inhibits squalene epoxidase: committed step

70
Q

Azoles inhibit ergosterol biosynthesis. What is the consequence?

A

Altered structure of function of the plasma membrane in fungi
> ergosterol acts as bioregulator of PM fluidity and asymmetry > membrane integrity

71
Q

Flucanazole resistance in AIDS patient can be dangerous, why?

A

Resistance builds up > dose increases > more dangerous side efffects

72
Q

Drawbacks current antifungals

A

-Limited number of antifungals available
-Amphotericin B is reversibly nephrotoxic
-Resistance against azoles in increasing

73
Q

Meningitis characteristics

A

-Infection with Exserohilum rostratum
-Spinal injections of steroids as pain relief, but steroids were infected with fungi

74
Q

Treatments meningitis

A

-Standard: Voriconazole
-Severe: Amphotericin B as well

75
Q

Why is the cell wall a good target for development antifugnal drugs?

A

Not in humans, and fungi depend on it for survival

76
Q

Ideal antifungal target characteristics

A

-Enzyme that synthesizes reaction product essential for viability funga; cell
-Enzyme is absent in humans or very different than human type

77
Q

Which cell wall components (polysaccharide components) of fungi can be targeted?

A

Synthesis of
-alpha-glucan
-beta-glucan
-chitin

78
Q

Cell wall composition

A

Long polysaccharides for rigidity and strength on outside of PM, proteins associated as well

79
Q

Enzymes for polysaccharides in fungal cell wall?

A

-Alpha-glucan synthase
-Beta-glucan synthase
-Chitin synthase

80
Q

Structure beta-glucan synthase and chitin synthase

A

Both are transmembrane proteins with catalytic domains located intracellularly

81
Q

Energetically enriched substrates of chitin synthase and beta-glucan synthase

A

Chitin synthase: UDP-N-acetylglucosamine
Beta-glucan synthase: UDP-glucose

82
Q

Chain growth chitin and beta-glucan

A

growth of the chain intracellularly
> useful UDP stays inside cell
> made chain (not the ends) are translocated to extracellular between the two transmembrane domains of either chitin/b-glucan synthase

83
Q

Competitive inhibitor of chitin synthase

A

Nikkomycin

84
Q

Nikkomycin function

A

Peptidyl nucleoside produced by a bacterium
> competitive inhibitor chitin synthase by mimicking UDP-acetylglucosamine
> contains reactive peptide bond
> potent antimycotic activity

85
Q

Caspofungin function

A

Prevent translocation of growing beta-glucan chain to extracellular side PM by the beta-glucan synthase

86
Q

Caspofungin is a … and these inhibitors work ….

A

Echinocandins > non-competitive inhibitors of beta-glucan synthase
> other used echinocandins: Anidulafungin and Micafungin

87
Q

Echinocandins kind of molecules ?

A

Lipopeptides
> many reactive peptide bonds
> integrate into channel and bind
> attaches to the synthase

88
Q

Alpha-glucan synthase at 37 degrees?

A

Is inactive, fungal cell dies
> 19 degrees: normal shape alpha-glucan synthase

89
Q

Structure alpha-glucan synthase

A

-Domain for linking alpha-glucan (extracellular)
-Transmembrane domain for alpha-glucan transport across membrane
-Domain for synthesis alpha-glucan (intracellular)

90
Q

The putative catalytic domains of polysaccharide synthases for the fungal cells wall are located …

A

intracellularly

91
Q

What if there is no alpha-glucan in the cell wall. Which fungus has a disadvantage if this happens?

A

The (protective) capsule cannot bind
> In Cryptococcus neoformans: required for normal growth and capsule binding: becomes invirulent
> In S. pombe: required for maintaining structural integrity

92
Q

HC39: Of what cells is the blood-brain barrier composed?

A

Endothelial cells of brain capillaries form the blood-brain barrier

93
Q

Blood-brain barrier forms barrier between ..

A

Blood and cerebral spinal fluid

94
Q

Where is the blood brain barrier located?

A

Throughout the whole brain: needs a lot of nutrients
> 20% oxygen consumption
> expensive organ

95
Q

Between the endothelial cells of the Blood-brain barrier, there are ….

A

Tight junctions

96
Q

GLUT transporters of ECs in blood brain barrier

A

GLUT1 (both sides)

97
Q

Transport FAs across blood brain barrier

A

Polyunsaturated FAs transported, not saturated

98
Q

Which molecules can pass the blood brain barrier by diffusion

A

Small molecules and gasses like CO2, H2O and O2

99
Q

Ion transport across blood brain barrier

A

Use of channels

100
Q

Transport from blood to brain

A

Blood > ECs > interstitial space > endfoots astrocytes

101
Q

How can drugs be transported across the blood brain barrier?

A

Piggyback transport with ABC transporters

102
Q

Transporters in blood brain barrier

A

-Glucose: GLUT1
-Lactate: Monocarboxylated co-transporter 1 (MCT1)
-Amino acids

103
Q

MCT1 transport

A

Lactate and proton cotransport (neutralize charge)

104
Q

How do transferrin, insulin and other proteins cross the blood brain barrier?

A

Receptor-mediated transcytosis
> endocytosis and exocytosis on other side EC
> requires receptors

105
Q

Membrane potentials neurons

A

-Lots of ion fluxes
-Resting membrane potential: -60 to -80 mV
-Cell interior has baseline negative voltage
-Graded potentials (dendrites and soma) and axon potentials (axons) transiently increase or decrease membrane potential

106
Q

Effect increased expression receptor proteins and ion channels on energy consumption of brain

A

Increases it

107
Q
A
108
Q

Neuron-astrocyte metabolic coupling using lactate

A

-Glucose uptake by ECs in blood brain barrier using GLUT1
-Uptake by either Astrocyte or neuron
Astrocyte (transastrocyte path)
> uptake by GLUT1
> Storage as glycogen
> or glycolysis to pyruvate to complete oxidation or to lactate
> Lactate cotransport with proton via MCT1 to interstitial space and again with proton into neuron via MCT2
Neuron
> Uptake glucose via GLUT3 or lactate via MCT2
> Glycolysis glucose or Lactate to pyruvate
> complete oxidation for energy

109
Q

Why the neuron-astrocyte metabolic coupling of glucose metabolism?

A

Storage glucose as glycogen in astrocytes (not so much in neurons)

110
Q

Why can T2DM induce mood disorders?

A

Insulin resistance
> Serotonin (5-HT) neurons express the insulin (Ins) receptor
> good mood

111
Q

Effect insulin on serotonin neurons

A

Promotes the synthesis of serotonin
> in T2DM: less synthesis because of insulin resistance

112
Q

T1DM and serotonin production

A

No insulin: no serotonin production in untreated T1DM

113
Q

Lipid metabolism in brain

A

Only uptake polyunsaturated FAs which are preferentially oxidized to form lipid peroxides
> Lipoxygenase (Fenton chemistry) makes hydroperoxide (5-HPETE) from arachidonic acid (shift extra double bond and oxidize -CH to -OOH)
> Intermediates: redicals.
> Steps: Hydrogen abstraction, rearrangement, O2 uptake with H+)

114
Q

Why are polyunsaturated FAs prone to oxidation

A

They contain methylene bridges > sensitive
> in the brain; only transporters polyunsaturated FAs, and a lot of oxygen available

115
Q

Why is it important that the lipoxygenase is in neurons?

A

So that the oxidation forming radicals does not occur

116
Q

Coupling lipid metabolism neurons-astrocytes

A

-Highly active neurons exocytose toxic lipid peroxides in apolipoprotein E (apoE) particles
> Astrocytes endocytose ApoE particles, incorporate the lipid peroxides into lipid droplets, detoxify them and use them as fuel in beta-oxidation (mitochondrial metabolism upregulated)

117
Q

-In the highly active neurons, high levels of ROS induce ??? of FAs

A

peroxidation

118
Q

Astrocytes produce ??? and detoxify and break down toxic fatty acids

A

anti-oxidants

119
Q

Important risk factor Alzheimers Disease, and protective factor?

A

Apolipoprotein E gene for late-onset AD
> Two cysteines (Cys) at 112 and 158 of ApoE: protection
> Both mutated to arginine (Arg): higher risk AD

120
Q

APOE2 and APOE4

A

-APOE2: ApoE isoform: 112 Cys 158 Cys > protective effect
-APOE4: ApoE isoform 112 Arg 158 Arg > most likely to develop AD
> most are APOE3 with one of each

121
Q

Glutamine-glutamate cycle in brain

A

Glutamine neurons take up glutamine and convert it to neurotransmitter glutamate using enzyme glutaminase
> Astrocytes can take up excess glutamate and convert it to glutamine using enzyme glutamine synthase (transamination).
> Glutamine cycled back to glutamine neuron using transporters
> Glutamate in synaptic cleft can also be taken up by glutamine neurons themselves (presynaptic)

122
Q

Why is glutamate important?

A

Crucial in cells

123
Q

Brain glucose level

A

Independent of blood glucose levels
> 2.0-2.5 mM: stable

124
Q

Formation glutamate and oxaloacetate in brain. What happens in hypoglycemic brain damage

A

From a-ketoglutarate and aspartate
> Hypoglycemic
> balance other way: oxaloacetate accumulates because glycolysis slows down and acetyl-CoA decreases
> Oxaloacetate + Glutamate > aspartate + a-ketoglutarate
(enzyme aspartate transaminase)
> promotion aspartate excretion by glutaminergic neuron

125
Q

Lafora disease

A

Carbohydrate binding phosphatase called Laforin is deficient
> accumulation highly phosphorylated less branched and water-insoluble glycogen called Lafora bodies in neurons and other glycogen synthesizing tissues.

126
Q

Problem phosphorylation glycogen

A

It is not normal
> due to mutation in carbohydrate binding domain of the phosphatase laforin
> abnormal glycogen
> accumulation Lafora bodies –> neurodegenerative disease Lofora disease

127
Q

Glycogen storages in brain

A

Astrocytes, and a little in neurons

Medical Biochemistry and Pathophysiology (16 decks)

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