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Tim's Cards > Microbiology I > Flashcards

Microbiology I Flashcards

1
Q

Name 5 ways to identify the presence of a pathogen.

A 
Direct Microbial Analysis
Cultivation
Antigenic analysis 
Genetic analysis
Detection of Immune response
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2
Q

What are the 4 Direct Detection methods of a pathogen?

A

Direct (needle in haystack)
Culture (isolated colonies from streaks)
Antigenic (antibodies exquisitely accurate)
Genetic (highly specific, very expensive)

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3
Q

What happens when the highly accurate detection of microbial antigens by antibodies works?

A

Agglutination

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4
Q

What is an Indirect Detection method for identifying a pathogen?

A

Measure an immune response

appearance of antibodies against a microbe

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5
Q

What are the 3 broad groups of infectious microbial agents?

A

Normal flora
Opportunists
Pathogens

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6
Q

What is another term for a pathogen?

A

Overt or Frank

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7
Q

What are 2 categories of opportunists?

A

Normal flora

Outsiders

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8
Q

T/F

Viruses can be considered part of the normal flora

A

False

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9
Q

Diagnostically, pathogens are usually identified through _____ or _____.

A

Tissue direct assay
Isolation and culture

(both followed by identification)

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10
Q

What antibody is present in an acute infection?

A

IgM

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11
Q

What is diagnostically relevant for pathogens if Convalescent?

A

Antibody types an [conc]

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12
Q

Name an acid fast bacteria and two diseases it causes.

A

Mycobacterium

TB and Leprosy

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13
Q

What does India Ink tell you about a bacteria?

A

Capsule presence

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14
Q

How is KOH useful in pathogenic determination?

A

Can confirm if its a Fungus

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15
Q

What type of Direct Visualization involves pre-labeled antibodies that fluoresce?

A

FITC Serology

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16
Q

An In Vitro culture of bacteria can be grown on what?

A 
Enriched media (augar)
Selective media

*Aerobic or Anaerobic

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17
Q

How are viruses cultured?

A

Eggs or cell culture

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18
Q

What are 2 enzyme tests used in pathogen identification.

A

Catalase

Oxidase

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19
Q

What are the 3 major life forms found on earth?

A

Archaea
Bacteria
Eukaryotes

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20
Q

What are the 3 Eucarya genera visible to the naked eye?

A

Zea, Homo, Coprinus

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21
Q

What are the 5 classes of infectious agents?

A 
Archaea
Bacteria
Eukaryotes
Infectious particles (viruses)
Infectious proteins (prions)
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22
Q

What are 3 main classes of Eukaryotic infectious agents?

A

Helminths (ascaris, enterobius)
Protozoa
Fungi

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23
Q

Name 3 protozoan pathogens.

A

Plasmodium (malaria)
Giardia (giardiasis)
Toxoplasma

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24
Q

T/F

Archaea are generally not found as human infectious agents.

A

False

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25
Q

What are 3 places Archaea are found in humans?

A

Colon
Pulp Chamber
one more? ask around

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26
Q

Name 2 infectious Prions

A

Mad cow

Kuru

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27
Q

What virus can withstand more environmental stress, enveloped or naked?

A

Naked

envelopes dry out

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28
Q

T/F

All bacteria have Fimbrae.

A

True

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29
Q

T/F

Bacteria divide at the same rate as Eukaryotes

A

False

bacteria fastest - 15 min.
Eukarytoic - around 12 hrs

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30
Q

What bacterial structure makes phagocytosis much more difficult?

A

Capsules

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31
Q

What is the capsule made out of?

A

CHO

carbohydrate

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32
Q

T/F

Prokaryotes have no ribosomes

A

False

but they are much smaller than eukaryotic

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33
Q

What type of Fimbrae binds bacteria to host or other bacteria?

A

Lectins

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34
Q

What is an important structural component of ECM?

A

CHO

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35
Q

Describe dsDNA.

A

Single circular plasmid

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36
Q

T/F

Bacteria can contain several plasmids

A

True

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37
Q

Size bacterial ribosome:

Size Eukaryotic ribosome:

A

70S

80S

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38
Q

What is the complex ecological biosystem of bacteria called?

A

Biofilm

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39
Q

What is a bacterial cell wall made of?

A

Polysaccharide chains cross-linked by peptides

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40
Q

What are the 2 glucose dimers that make up bacterial cell walls?

A

N-acetylglucosamine (NAG)

N-acetylmuramic acid (NAM)

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41
Q

What fixes the NAG/NAM/peptide complex to a cell wall in synthesis?

A

Transpeptidase

these “spot weld”

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42
Q

What is constantly synthesizing and degrading peptidoglycan?

A

Autolysins

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43
Q

What additional features does Gram Negative bacteria have?

A

Periplasmic space
Outer membrane
Endotoxin (LPS)

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44
Q

A gram negative can’t hold its alcohol.

explain.

A

Gram Negative bacteria lose Cresyl Blue when EtOH applied

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45
Q

How many Toll-like receptors are there?

What is the Toll-like receptor that binds LPS?

A

10

TLS-4

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46
Q

T/F

Toll like receptors are highly specific

A

False

They are “pattern recognition” so are broadly acting

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47
Q

What cytokine affects Endothelial cells in the LPS > TLS-4 cascade?

A

TNF

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48
Q

What are the characteristics of systemic LPS pathology?

A 
Intravascular coagulation (blockage)
Hypovolemic shock (from decreased BP)

Hypovolemic = Septic

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49
Q

What do macrophages secrete in response to LPS?

A

Proteases (breakdown ECM and collagen)
PGE-2
TNF

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50
Q

What relaxes pre-capillary sphincters?

substance/cell/cytokine

A

NO
by Endothelial Cells
signalled by TNF-alpha

*can be activated by LPS > TLR-4

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51
Q

What is PGE-2 effects on bone?

A

Signals resorption

*Osteoclast activity

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52
Q

What is PAMP and DAMP?

functions?

A

Pathogen recognition
(aid WBC’s)

Damage recognition
(allow for recognition of damaged cells so PMN’s can remove)

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53
Q

What division of immunity are PAMP and DAMP in?

A

Native Immunity

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54
Q

What is the most important pro-inflammatory mediator stimulated by Toll-like Receptors?

A

TNF-alpha

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55
Q

What type of enzyme breaks linkages in starch/glycogen?

A

Amylase

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56
Q

What type of polysaccharide is structural?

A

Cellulose

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57
Q

What type of enzyme breaks peptidoglycan?

A

Lysozyme

*at NAM-NAG linkage

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58
Q

How is Chitin related to Peptidoglycan?

A

chitin: Beta 1-4 NAG
peptidoglygan: Beta 1-4 NAG-NAM

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59
Q

T/F

ECM is made up of glucose molecules stuck in polymer.

A

True

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60
Q

Why does penicillin not harm human cells?

A

It targets peptidoglycan and humans don’t have cell walls

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61
Q

What are the 3 steps of effective penicillin action?

A
  1. Bacteria must be growing, using autolysin enzymes called hydrolases
  2. Blockage of “spot welding” by binding Transpeptidase
  3. Lysis by osmotic pressure
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62
Q

What would happen if penicillin were added to cells growing in an isotonic solution?

A

???

Probably wouldn’t burst but would continue to degrade

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63
Q

What type of antibiotics kill bacteria?

What type inhibit their proliferation?

A

Bacteriocidal

Bacteriostatic

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64
Q

Why does bacteria use right handed D-AA’s in their cell walls?

A

We digest only L-AA’s

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65
Q

What type of structure is penicilin?

A

Beta-Lactam Ring

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66
Q

What are 4 methods bacteria have developed to resist Penicillin?

A

Destroy, Divert, Morph, Stop growing

Penicillin-ase
Pump Penicillin out (outer) membrane
Change shape of Transpeptidase
Decrease Hydrolase Activity

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67
Q

What is a side effect of Penicillin’s unstable Beta-lactam ring?

A

Can induce immune response by binding self-proteins
(like platelets, RBC’s, macrophage)

*a hypersensitivity

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68
Q

What is a facultative bacteria?

A

Can Respire (O2, Heme) or Ferment

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69
Q

What is an aerotolerant anaerobe?

What is a microaerophilic anaerobe?

A

Can tolerate O2 but only ferments

Thrives in low level O2

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70
Q

What is the function of Super Oxide Dismutase?

What is the function of Catalase?

A

O2- > H2O2

H2O2 > H2O and O2

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71
Q

What 2 enzymes do Obligate aerobes and facultative aerobes have in order to deal with the side effects of Oxygen?

A

Super Oxide Dismutase

Catalase

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72
Q

Why do strict anaerobes die in the presence of Oxygen?

A

Don’t have Super Oxide Dismutase or Catalase `

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73
Q

Clinical periodontal practice is often aimed at reducing what pathogen?

A

Sub-gingival Anaerobes

74
Q

What 3 ways can bacteria exchange genetic material?

A

Transformation: Free DNA slurped
Transduction: Viral transfer
Conjugation: Direct transfer

75
Q

T/F

A plasmid is the dsDNA of a bacterial cell.

A

False

Plasmid is only part/small pieces and optional and are spread intra and inter cellularly by several means

76
Q

What is the most common mutational change in the cell?

A

Point mutation

77
Q

Name 3 types of Base Replication Errors.

A

Point mutation
Base Deletion
Base Insertion

(latter two are frameshift and often fatal )

78
Q

What is a rare but extremely important type of mutation?

A

Gene duplication

79
Q

What are our 2 major (broadly speaking) defense systems?

A

Innate immunity and Adaptive immunity

80
Q

Where do all the blood cells and platelets arise?

A

Stem cells in marrow

81
Q

Innate and adaptive’s actions in terms of Specificity, Speed, and Memory.

A

Innate: broad, fast, no
Adaptive: very slow (1st time), yes

82
Q

Inflammation is part of the _____ immune system but stimulates the _____ immune system.

A

Innate

adaptive

83
Q

What are 3 Inflammatory response organs?

A

Brain - fever
Liver - mark cells for death
Marrow - WBC

84
Q

3 signs Acute Inflammation

3 signs Chronic Inflammation

A

Plasma Proteins, Mast cells, neutrophils

Cell proteins, lymphocytes, macrophage

85
Q

What molecule is released from Sentinel (mast) cells?

86
Q

What are the “stop signs” in capillary cells in response to inflammation?
(these allow inflammatory response cells to enter tissue)

A

cell adhesion molecules

CAMs

87
Q

Why does material travel slowly through the lymph?

A

increases chance antigen finds specific lymphocyte

88
Q

What are the primary lymph tissues?

A

Marrow and Thymus

89
Q

Where are B and T cells ‘educated?’

A

B - marrow

T - Thymus

90
Q

5 Secondary lymph tissues:

A 
lymph nodes 
spleen
adenoids
tonsils
Peyer's patches
91
Q

What type of receptors are on B-cells?

A

Ag (antigen) - specific

aka B cell receptor (BCR)

92
Q

What are Antibodies (immunoglobulins)?

A

released copies of B-cell receptors specific to certain antigens

*this coats and flags antigens

93
Q

Define TCR.

Function?

A

T-cell receptor

unlike B-cell, does NOT leave cell surface

only binds to “processed protein” on surface of other cells

94
Q

Once a TCR binds a processed protein, what is the next step?

A

Releases Cytokines

95
Q

What region of antigen binds to TCR, BCR?

How big?

A

Epitope

5-10 AA’s

96
Q

Define Antigen:

A

Any molecule “seen” by BCR or TCR.

97
Q

Other than BCR’s and TCR’s, what can protein antigens bind to?

A

HLA (Human Leukocyte Antigen) presenter proteins

98
Q

What are some pathologies of Strep pneumoniae?

*remember, this is Gram +

A

Pneumonia
Ear aches (toddlers)
Meningitis

99
Q

Why are capsules immunogenic (inductive of adaptive response)?

A

Coated with antibodies and Opsonized for Phagocytosis

100
Q

When capsules are opsonized, what binds to phagocytes?

A

Fc portion to Fc receptors on phagocyte

101
Q

T/F

Strep pneumoniae has a capsule

A

False
can have capsule or not
*most often has a CHO capsule

102
Q

What is the function of the CHO capsule in Strep. pneumoniae?

A

protects from phagocytosis (major virulence factor)

103
Q

How are bacteria with CHO capsule dealt with?

A

B cell binds, internalizes, chops up, and presents to HLA (lymphocyte)
T cell recognizes HLA presenter, releases cytokines

T and B cells then divide into CLONES
B cell makes antibodies

104
Q

What type of antibody do we produce the most of?

A

IgA - more than all others combined

105
Q

T/F

All gram positive bacteria have endotoxin, some have exotoxin

106
Q

T/F

Gram positive bacteria have no endotoxin

107
Q

T/F

Endotoxin is secreted

A

False

in contrast to exotoxin

108
Q

Most of the normal gut flora is made up of what?

What does this do?

A

Gram negative rods

low level leakage of LPS develops our immune system

109
Q

What are 3 types of exotoxins?

A

Cytolytic - punches holes in membranes
A-B toxins - causes cell dysfunction and death
Superantigens - cytokine storm

110
Q

What recognizes LPS?

111
Q

Lipid prostaglandin, leukotriene mediators, and protein enzymes can be produced by what?

A

Activated macrophage

112
Q

What macrophage receptor can Gram + peptidoglycan affect?

A

TLR-2

*generally less potent

113
Q

What does LPS activate directly (3 things)?

this is why innate system can take care of low level Gram-

A

Hageman factor - coagulation
Platelets - also coagulation
Macrophage - O2-, cytokine, etc

114
Q

What does Gram negative cause in large numbers if in the blood?

A 
Hypovolemic shock (CV failure)
Intravascular coagulation (organ shutdown, ARDS)

*this comprises Sepsis

115
Q

What do monocytes/macrophage “drool”?

A

Proteases (breakdown ECM/collagen)
PGE-2
TNF-alpha

116
Q

Because it’s been in notes multiple times, what is an important function of TNF-alpha?

A

Signals NO production relaxing pre-capillary sphincters

117
Q

What are the 3 ways of categorizing exotoxins by action?

A

Cytolytic - hole punching
A-B toxins - binds to specific host cells
Superantigens

118
Q

What are the most toxic substances known?

How do they work?

A

A-B toxins

as enzymes

119
Q

How does the Shigella A-B toxin work?

A

cleaves ribosomal RNA

120
Q

How does a Superantigen initiate a cytokine storm?

A

Incorrectly binds antigen to TCR to HLA class II molecule on APC’s (antigen presenting cells)

121
Q

How do superantigens affect the sensitivity to LPS?

A

Increase 100x

122
Q

What are the 2 major pathological Gram + cocci?

A

Streptococci

Staphylococci

123
Q

Major strep pathogen?

A

Strep pyogenes

124
Q

Major staph pathogen?

A

Staph aureus

125
Q

How does Strp pyogenes avoid detection?

A

Incorporates host proteins

126
Q

Sterptococcus pyogenes are histological ______ and Staphylococcus aureus are ______

A

Chains

Clusters

127
Q

What gram + pyogenic cocci can use oxygen?

A

Staphylococcus aureus

128
Q

Compare outer layer of Streptococcus pyogenes and Staphylococcus aureus.

A

Strept - incorporates host protein

Staph - secreted binds Fc (covers up opsonin)

129
Q

Bad case of Strept p. leads to…

A

Scarlet/Rheumatic fever

130
Q

T/F

flesh eating bacteria can be either strept or staph

131
Q

Bad case of Staph aureus can lead to…

A

Toxic shock

132
Q

T/F
Staph are aerotolerant
Strept are facultative

A

False
Staph are facultative
Strept are aerotolerant

133
Q

T/F

Streptococcus are small, white, and non-motile

134
Q

T/F

Streptococcus are found in chains or pairs

135
Q

What 4 species of Streptococcus cause most diseases?

A

Pyogens
Agalactiae
Pneumonia
Viridans

136
Q

How does Streptococcus grow in vitro?

A

Fastidious (kind of picky)

137
Q

Do Strept use catalase?

138
Q

Are strept resistant to antibiotics?

139
Q

Strept do well in microaerophilic conditions

140
Q

A relationship good for both organisms is…

141
Q

What group of Streptococcus are opportunistic oral flora?

142
Q

What are the 3 Pyogenic Streptococci?

A

pyogenes
agalactiae
pneumonia

143
Q

Hemolysis categories:
Beta
Alpha
Gamma

A

Beta - complete lysis
Alpha - partial lysis
gamma no lysis

144
Q

What is the major bacterial species in the oral cavity?

A

Alpha hemolytic Streptococcus viridans

145
Q

What are the 2 Pyogenic Strept?

What are the 2 Viridans Strept?

A

S. pyogenes
S agalactiae
(Beta hemolytic)

S. pneumoniae
Viridans Strep.
(alpha hemolytic)

146
Q

Describe S. pyogenes?

A

Beta hemolytic, Group A

strept throat, rheumatic fever

147
Q

What Strept is the normal flora of the vagina?

Describe classifications

A

S. agalactiae

Beta hymolytic, Group B, Capsule

148
Q

What Strept causes meningitis?

A

S. pneumoniae

alpha hemolytic, capsule

149
Q

What are the Gamma hemolytic group?

A

Enterococcus

150
Q

What 2 bacteria cause endocarditis?

A

S. pyogenes

Viridans Strep

151
Q

What varies in the 150 strains of Strep pyogenes?

A

M proteins

152
Q

What does Strep pyogenes produce that kills leukocytes and destroys clots?

A

Streptolysins

153
Q

How does Strep pyogenes shut down Complement?

154
Q

S. pyogenes can cause what condition in which bacteria moves throughout tissue?

A

Cellulitis

155
Q

What 2 types of exotoxin does S. pyogenes produce?

A

Cytolytic

Superantigen

156
Q

What are 3 forms of disease caused by S. pyogenes?

A

Local pyogenic - strep throat, impetigo, cellulits

Toxic systemic - scarlet fever (10% untreated), STSS

Immune Sequelae - Rheumatic fever (cross reactive, type II) Glomerulonephritis (type III hypersensitivity)

157
Q

Toxic systemic disease caused by S. pyogenes is caused by?

A

Superantigen

*note - systemic, so damage occurs away from infection

158
Q

What is the type II hypersensitivity caused by S. pyogenes?

Type III?

A

II - Rheumatic fever

III- Glomerulonephritis

159
Q

Type II hypersensitivity (like Rheumatic fever) result from?

A

Direct binding of antibody to epitope on host tissue

160
Q

Type III hypersensitivity (like glomerulonephritis) results from?
What interstitial complexes perform the same process?

A

Innocent bystander damage via Complement

Arthus Rxns

161
Q

What type of damage is Rheumatic fever?

A

Type II hypersensitivity

162
Q

What causes Glomerulonephritis as a result of S. pyogenes infection?

A

Ab-Ag complex binds in glomerulus

Type III damage

163
Q

Explain Viridans Strep cause of sub-acute bacterial endocarditis?

A

Prior heart damage leaves it “sticky”

164
Q

What two pathogens cause acute infective endocarditis?

A

S. aureus

S. pyogenes

165
Q

What 2 opportunists cause sub-acute infective endocarditis?

A

Dental Viridans

Gram negative enterics

166
Q

A previously damaged heart is necessary for these 3 things to cause further damage:

A

Staph from drug abuse
Dental viridans
Surgery/Enterics

167
Q

General characteristics of Staphylococcus:

A

Gram +
Very Hardy
Catalase +
Facultative

168
Q

What 3 Staphylococcus cause most infections?

A

S. aureus
S. epidermidis
S. saphrophyticus

169
Q

What Staph is Coagulase+?

170
Q

What Staph has exotoxin?

Which causes UTI’s?

A

S. aureus

S. saprophyticus

171
Q

T/F

Staph has the nasal cavity to itself.

172
Q

What are 4 virulence factors of S. aureus?

A 
Protein A (blocks opsonization by binding Fc)
Fibrin binding
Enzymes (spreading factors destroy ECM)
Cytolytic toxins
Superantigens
173
Q

What causes Scalded Skin Syndrome in children?

A

A protease (exfoliative toxin) of S. aureus

174
Q

How does Protein A work?

A

Binds Fc (on IgG) so receptors can’t find Staph

175
Q

How does coagulase work to benefit S. aureus?

A

Causes fibrin to form a wall around infection.

*Abscess diseases

176
Q

T/F

Stapholococcus aureus is a very strong pathogen

A

False

despite all its tricks

177
Q

Why does S. aureus cause a “true” food poisoning?

A

The toxin, instead of the bacteria, is the culprit

*toxins very heat stable

178
Q

Some tampons can cause…

A

TSS - toxic shock syndrome

*S. aureus

179
Q

Toxic shock like syndrome is caused by…

A

Streptococcus pyogenes

180
Q

Nosocomial:
Iatrogenic:

A

hospital acquired

doctor acquired

181
Q

How does Staph share resistance factors?

A

Promiscuous conjugation

Tim's Cards (140 decks)

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