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Mycology > Intro > Flashcards

Intro Flashcards

1
Q

What parts of a fungal cell wall are important?
5 parts
(man, kite, b-garbagecan, ergs, mic.)

A

Mannan (polymere of manose)
B glucan & chitin
Ergosterol (like our cholesterol)
Mycolic

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2
Q

Main differences between yeasts and molds?

A

Mold: multi cellular, thread like, hyphae, mycellium
Yeast: single cell, anaerobic, creamy like bread yeast,

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3
Q

What is a germ tube?

A

Candida ablibicans makes this. Tube of yeast that looks like a hypha but is a yeast tube.

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4
Q

What is a Pseudohypha?

A

A fake hypha made by yeast

Tiny balls that branch out

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5
Q

What is a bud?

A

AKA blastoconidia

made by yeast

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6
Q

What are the main species of candida?

Albus Dumbledore got thrush and balanitis and started to “glab” about his vaganitis.

A

C. albicans, C. glabarata

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7
Q

Where species candida mainly found?

A

skin, mouth, upper resp. tract, bowel, vagina

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8
Q

What is balanitis?

A

Fungus (candida) in the foreskin –> swelling of foreskin and head of penius

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9
Q

What is thrush?

A

Candida (yeast) infection on the tongue

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10
Q

What is vaginitis?

A

Candida (yeast) infection on the vagina

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11
Q

What causes diaper rash?

A

Candida (yeast) infection

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12
Q

What can cause intra-abdominal abscesses by yeast?

A

Candida (yeast) infection

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13
Q

Where are common infections of candida (yeast)?

A

Thrush, vaginitis, balanitis, diaper rash, esophagitis, intra-abdominal abscesses, blood stream infection

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14
Q

What makes a dimorphic fungi?

A

Mold at cool temps
Yeast at high temps

  • geographically restricted
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15
Q

What is an example of a dimorphic fungi?

Gold miner

A

Coccidiodes immitis/posadasii

- endemic for a certain area

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16
Q

What is an opportunistic pathogenic fungi?

A

Takes advantage of a weak or compromised host

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17
Q

What are the examples of opportunistic fungi?

- hold a “candle” so “rhino” doesnt kill you

A

Candida spp.

Rhizopus spp.

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18
Q

What is the approximate slide of viruses?

A

20-300nM in Diameter – SMALL/TINY

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19
Q

What are the main components of a virus?

A

Nucleic acid
Protein
*may have Lipid Envelope

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20
Q

How do viruses replicate?

A

Obligate intracellular parasites

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21
Q

Basic components of a virus?

A

Genome (RNA or DNA)
Capsid (icosahedral, helical)
Integument
* if enveloped: membrane + glycoproteins

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22
Q

On an envelope what purpose do the glycoproteins have?

A

to bind to cellular receptors

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23
Q

What are the oncogenic viruses?

Baseball game: Pitcher, catcher, T ball, fans, outfielders

A 
Human papillomavirus (HPV): cervical ca
EBV: lymphoma, nasopharyngeal ca
KSHV: kaposi sarcoma, lymphoma,
Hep. B/C viruses: hepatocellular ca
HTLV-1: T cell lymphoma
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24
Q

Tumor supressor genes targeted by viruses?

P’s, Retina, E’s

A

p53
Retinoblastoma protein (Rb)
E6 takes out p53, E7 takes out retinoblastoma

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25
Q

Gram + cell wall components

Think PPP

A

Peptidoglycan, Purple, Positive
Teichoic acid
One cell wall

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26
Q

Gram - cell wall components

A

LPS Layer (toll-like receptor binds here)
Outer membrane
Periplasmic space
Cytoplasmic membrane

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27
Q

Key unique features of bacteria?

A

Single, or circular, and may have plasmids
No organelles
No nucleus
Cell wall (G- or G+)
70s ribosomes (targeted in drugs) (eukaryote has 80s)
Metabolic pathways differ
Mode of replication (Binary fission)

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28
Q

What microbes are eukaryotic?

A

Molds and yeasts

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29
Q

What are important features of a mycobacterium?

A

Mycolic acid in its cell wall

Acid fast: means when stained then we will see RED

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30
Q

What is an important mycobacterium to remember?

A

Mycobacterium Turberculosis

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31
Q

Tuberculosis causes what in the lungs?

A

Ghon complex: old calcified tissue from TB infection

- may contain viable latent bacteria that can become reactivated

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32
Q

Where does primary vs secondary TB occur?

A

Primary: lower lobes of the lungs
Secondary: upper lobes of the lungs

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33
Q

MTB is spread how?

A

Via aerosoles

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34
Q

How do they test for MTB?

A

Delayed type hypersensitivity

- If you have the infection then a response will be seen when given injection

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35
Q

What is caseous necrosis?

A

When cell death happens caused by progessive enzymatic degradation. A caseous material remains and then is calcified to make ghon complex

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36
Q

If you get MTB what is the chance that the mycobacterium becomes latent?

A

90-95% chance

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37
Q

Is latent MTB contagious?

A

No

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38
Q

What types of patients if once infected will see secondary MTB?

A

The immunocomprised

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39
Q

When looking in histoligical stain how will you recognize MTB?

A

It will be red –> ACID FAST

NOT BLUE –> other bacteria

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40
Q

What mycobacteria species are important to know?

A special “leprous” “fortune teller” lives in “kansas”. He has a love for “aviation” but he uses for “tuber” potatoe for his airplane… he cant fly because his “tuber” potatoe aiplane has a rapidly growing “abscess”.

A
  • Mycobacterium tuberculosis
  • Slower growers:
    • M. avium-intracellular
    • M. Kansasii
  • Rapid growers:
    • M. chelonae-abscessus
    • M. fortuitum
  • Special grower:
    • M. Leprae
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41
Q

What is needed for +ssRNA to be made into mRNA?

A

Nothing

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42
Q

What is needed for -ssRNA to be made into mRNA?

A

Virion RdRp

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43
Q

What is needed for +/-ssRNA to be made into mRNA?

A

Virion RdRp

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44
Q

What is needed for dsRNA to be made into mRNA?

A

Virion RdRp

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45
Q

What is needed for retrovirus to be made into mRNA?

A

Reverse transcriptase –> DNA (Inserted in gemome) –>

RNA polymerase of cell

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46
Q

What is needed for delta virus to be made into mRNA?

A

Cellular RNA polymerase

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47
Q

Define antigenic shift:

A

bigger change with whole segment movement between viruses. (2 viruses, one host)

Change not as abrupt.

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48
Q

Define antigenic drift:

A

slow change produced by point mutations.

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49
Q

What is segmented recombination?

A

It is 2 viruses in one host that exchange or recombine genetic information.

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50
Q

What is used to bind a virus to host cell membrane?

A

Haemagglutinin

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51
Q

How is a virus released from a cell?

A

Via budding with Receptors (specific) or attachment factors (not specific)

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52
Q

How does a virus typically enter a cell?

A

Via endocytosis

  • then into endosome
  • cues release it
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53
Q

How do enveloped viruses get released out of endosome?

A

Via cues such as pH, or proteases

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54
Q

How do non-enveloped viruses get release out endosome?

A

Via puncture, perforation, or lysis

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55
Q

How does a virus establish latency?

A

Existing as a plasmid and being intermittently transcribed. Also, it can be inserted in hosts DNA.

56
Q

How does a latent virus get reactivated?

A

It is changed from a plasmid to linear genome

57
Q

Where does VZV and HSV become latent?

chicken coop and dad

A

Epithelial cells and neurons

58
Q

Where does CMV become latent?

Duck with big head eats white blood

A

Ductal epithelium and leukocytes

59
Q

Where does EBV become latent?

Einstein and the pharaoh suck limes

A

Oropharyngeal epithelium and B lymphocytes

60
Q

Where does KSHV become latent?

Kaposi throws lime foam and lives in End…

A

Endothelium and B lymphocytes

61
Q

What is considered point mutation?

A

Insertion or deletion

62
Q

What is bacterial transformation?

A

Horizontal gene transfer: where dead bacteria is eaten and the bacteria that does the eating acquires dead bacteria traits.

63
Q

What is bacterial transduction?

A

Horizontal gene transfer: where a bacteria transducts genetic material through a virus

64
Q

What is bacterial conjucation?

A

Horizontal gene transfer: where to bacteria have sex and transfer plasmids

65
Q

What is vertical gene transfer?

A

From parent to offspring

66
Q

What processes of genetic change are slow?

A

Point mutation, Gene duplication, Gene deletion, Chromosome rearrangement

RANDOM ERRORS ON CHROMOSOME

67
Q

What processes of genetic change are fast?

A

Phase variation (Changing phases allows you to adapt and attack better, turning on or off a gene)

Antigenic variation (change surface antigens to avoid host response)

HGT

68
Q

What types of HGT are there?

A

Intergenic recombination

  • Transformation: Plasmids, exogenous DNA
  • Congugation: plasmid, transposon

Transduction
- Phage: Generalized and Specialized

69
Q

Staphylococcus characteristics?

A 
G+
Sheep blood agar + 
Chocolate agar +
Colistin Naladixic acid + 
MacConkey Agar -
70
Q

Pseudomonas characteristics?

A 
G-
Sheep blood agar +
Chocolate agar +
Colistin Naladixic acid -
MacConkey Agar +
71
Q

E. coli characteristics?

A 
G-
Sheep blood agar + 
Chocolate agar +
Colistin Naladixic acid -
MacConkey Agar +
72
Q

Haemophilus characteristics?

A 
G-
Sheep blood agar -
Chocolate agar +
Colistin Naladixic acid -
MacConkey Agar -
73
Q

What does the MacConkey agar show?

A

Growth of gram neg.

74
Q

What does the Colistin Naladixic Acid agar show?

A

Growth of gram pos.

75
Q

What are the steps of staining?

A

1) Crystal violet
2) Iodine
3) Alcohol
4) Safranin

76
Q

Whats the morphology and gram stain for staphylococcus?

A

G+

Coccus

77
Q

Whats the morphology and gram stain for streptococcus?

A

G+

Coccus

78
Q

Whats the morphology and gram stain for bacillus?

A

G+

Bacillus

79
Q

Whats the morphology and gram stain for corynebacterium (diptheroid)?

A

G+

Bacillus

80
Q

Whats the morphology and gram stain for neisseria?

A

G-

Cocci or diplococci

81
Q

Whats the morphology and gram stain for Pseudomonas?

A

G-

Bacillus

82
Q

Whats the morphology and gram stain for E. coli?

A

G-

Bacillus

83
Q

Whats the morphology and gram stain for Candida albicans?

A

Coccus/ (Purple)

Yeast

84
Q

Whats the morphology and gram stain for Haemophilus?

A

G-

bacillus/coccus

85
Q

What is a protozoa?

A

Motile unicellular eukaryotic organisms that can become parasitic

86
Q

What are the 6 protozoa we need to remember?
(“a can of amoebas” are put on a “leash in the van”, the driver of the van is “toxic Ghandi” and his “glaring fowl” duck named “Bruce” and they are “cruzi’ing” down the road.)

A 
Acanthamoeba sp (a can of amoeba's)
Leishman donovani (leash in the van)
Toxoplasma gondii (toxic Ghandi)
Naegleria fowleri (glaring fowl duck)
Trypanosoma brucei (duck named Bruce)
Trypanosoma cruzi (Cruzi'ing down the road)
87
Q

What are the three types of inflammation to know, and in order of how much time it takes to develop?

A

Acute
Chronic
Granulomatous

88
Q

What cells stimulate “acute” inflammation?

A

Neutrophils
vessels
mast cells

89
Q

What cells stimulate “chronic” inflammation?

A

Lymphocytes
Macrophages
Plasma cells.

90
Q

What cells stimulate “granulomatous” inflammation?

A

Epithelioid histiocytes
Giant cells
Lymphocytes

91
Q

What’s the difference between “primary” and “secondary” lymphoid organs?

A

Primary: where the immune cells, b and t, are formed (bone marrow, thymus)
Seconary: where the immune response occurs (lymph nodes, spleen, peyers patches, appendix)

92
Q

How long does the innate vs adaptive immune response take?

A

innate: quick
adaptive: slower

93
Q

Is a Toll Like Receptor an “innate” or “adaptive” immune receptor?

A

Innate

94
Q

How do the innate and adaptive immune responses function together?

A

Macrophages (innate) grab antigens and take it to the lymph for B and T cells to process and use cytokines to signal the rest of the body to get working on an immune response.

95
Q

Difference between “innate” and “adaptive” immunity in terms of “specificity of receptors” and “clonality of receptors”

A

Innate: receptor not very specific…….they don’t clone new ones.
Adaptive: Receptors are very specific……they clone the receptors that work for new microbes

96
Q

What defective enzyme causes a “chronic granulomatous disease”?

A

a defective NADPH oxidase (won’t allow the macrophages to create a superoxide burst)

97
Q

What part of the genome causes “chronic granulomatous disease”?

A

GP 91

98
Q

What part of the population is most likely to get “chronic granulomatous disease” and why?

A

Males because it’s an X-linked trait.

99
Q

What Toll like receptors are found intracellularly? and what are they receptors for?

A

TLR 3,7,8,9

Viral nucleic acids

100
Q

What Toll like receptors are found extracellularly? and what are they receptors for?

A

TLR 1,2,4,5,6

Bacterial microbes

101
Q

What is a PAMP?

A

Pathogen Associated Molecular Patterns

102
Q

What role does NF kbeta play?

A

It’s involved in Cytokine production for immune cell activation

103
Q

What’s an antiviral cytokine to remember?

A

IFN a/b

104
Q

What are the three inflammatory cytokines activated by NF kb?

A

TNF
IL-1
IL-12

105
Q

How do HLA (or MHC class 1) interact with NK cells?

A

They inhibit the NK cell from killing them

106
Q

How does a MIC ligand affect a NK cell?

A

It activates it to kill it.

107
Q

What are the three components in the JAK STAT pathway?

A

membrane receptor
JAK (janus kinase)
STAT (signal transducer and activator of transcription)

108
Q

What’s the purpose of the JAK STAT pathway?

A

to help up-regulate certain immune responses, helps produce cytokines

109
Q

What are the 5 cytokines to remember?
(There’s a Natural Killer on Isle 12 (IL-12) with fiery dynamite that causes lots of bleeding (TNF-a). He’s looking for his ex-girlfriend (CXCL-8) who broke up with him after recruiting 8 new boyfriends. His ex-gf is hiding on isle-6 with a feverish liver. She moves to isle-1b to get better access to effector cells and blood.

A

IL-6 (fever, induces acute phase proteins by liver)
TNF-a (vascular permeability, Fever)
IL-1b (activates vascular endothelium, activates lymphocytes, local tissue destruction, Fever)
CXCL-8 (chemotactic factor, recruits neutrophils)
IL-12 (activates NK cells)

110
Q

What does properdin do? complement pathway?

A

On alternative pathway: it stabilizes C3BbB so it can “amplify” and create more C3b

111
Q

What’s the purpose of Factor H and Factor I? complement pathway

A

It inhibits the C3b pathway so you don’t run out of C3b.

112
Q

What is the convertase for C5?

A

2 of the C3b’s

113
Q

What happens if you have a C8 deficiency in the MAC?

A

recurrent Neisseria (encapsulated) infection

114
Q

What creates the MAC complex?

A

C6,7,8,9

115
Q

How is the MBL or Classical pathway C3 convertase structured?

A

C4bC2b

116
Q

What’s the MBL pathway?

A

IL-6 is produced by macrophages, goes to the liver, liver produces MBL, fibrinogen, and Acute phase proteins, The MBL binds to a microbe and attaches MASP which cleaves C4, C4b then attaches to the microbe, C2 is then cleaved and attaches to C4

117
Q

How does the classical pathway activate?

A

bound antibody. (multiple needed, IgM is the best)

118
Q

What are the 2 types of c5 convertase?

A

Alternative: C3b(2)Bb

MBL/Classical: C4bC2bC3b

119
Q

What’s an anaphylatoxin?

A

C3a

C5a

120
Q

What does CR1 do (complement receptor)?

A

Macrophages attach and eat it

RBC’s also have it to take microbes to the liver

121
Q

Why is CR2 (complement receptor) important?

A

It helps activate B cells

122
Q

What does CR 3,4 do?

A

Stimulates phagocytosis

123
Q

What does the Kupffer cell (liver) receive from RBC?

A

the bacterium attached to CR1

124
Q

When C1 inhibitor doesn’t work how expensive is the treatment for keeping swelling down?

A

$350,000 per year!!!!!

125
Q

What role does DAF play on host cells with Complement pathway?

A

It decays the convertase so it doesn’t destroy the host cell.

126
Q

How does CD59 and S protein work with the MAC?

A

CD59: inhibits the C9 pore

S protein: inhibits c5,6,7 insertion stuff

127
Q

If you don’t have CD59 what happens?

A

Random lysis of RBC’s.

128
Q

What are the key points for Rhizopus?

A

rare, High glucose, acidic, Ketoacidosis.

129
Q

What are the 3 oxidative burst enzymes?

A

NADPH oxidase
Superoxidase dismutase
Catalase

130
Q

What disease is caused by not having effective oxidative burst enzymes?

A

Chronic Granulomatous disease

131
Q

What is important about the TLR 4?

A

it recognizes LPS gram negative bacteria

132
Q

What cassettes are in the heavy chain sequence?

A
  1. D-j

2. V-D-J

133
Q

What cassettes are in the light chain sequence?

A

V-J

134
Q

What is RAG involved in?

A

recombination of immunoglobulins, for antibody production

135
Q

What’s the ABT parts of a toxin?

A

B: binds to the cell and gets pulled in (endosome)
T: makes a drill and breaks out of the endosome
A: is the activator part that messes with the host cell.

Mycology (1 decks)

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