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Clinical Micro > 101 Review and Catalase Neg. GPC- Streptococcus > Flashcards

101 Review and Catalase Neg. GPC- Streptococcus Flashcards

1
Q

Used to categorize and identify bacteria

A

Dichotomous flowcharts

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2
Q

Indicate preferential environment

A

Biochemical capabilities

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3
Q

CSF, aveoli, bladder, and body fluids/tissue are generally (BLANK) zones of normal microbiota

A

Axenic

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4
Q

The stomach generally has (BLANK) levels of normal microbiota

A

Low, Axenic

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5
Q

The (BLANK) & (BLANK) have some of the highest levels of normal microbiota

A

Mouth and colon

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6
Q

The hosts first line of defense

A

Microbial competition (i.e. normal microbiota)

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7
Q

Opportunistic pathogens are caused by…

A

Normal microbiota

  • in atypical locations
  • in immunocompromised
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8
Q

Primary pathogens are caused by…

A

Non-normal microbiota

-introduced through some portal of entry

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9
Q

Exoenzymes cause cell death by disrupting (BLANK) & (BLANK)

A

Host structures and permeability barriers

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10
Q

Signs are (BLANK) evidence, noted by (BLANK)

A

Objective, others

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11
Q

Symptoms are (BLANK) evidence, noted by (BLANK)

A

Subjective, patient

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12
Q

Signs and symptoms can help to identify (BLANK) & (BLANK)

A

Etiological agent, site of growth

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13
Q

(BLANK) are usually metabolically crippled and need host growth factors

A

Obligate intracellular pathogens

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14
Q

Cells that grow separate from biofilm are called…

A

Planktonic cells

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15
Q

Biofilms protect microbes from (BLANK) & (BLANK)

A

Antibodies and phagocitic cells

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16
Q

GNB use (BLANK) as autoinducers

A

AHL (lactones)

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17
Q

GPB use (BLANK) as autoinducers

A

AIP (peptides)

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18
Q

Quorum sensing alters transcription by…

A

Two component regulatory systems

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19
Q

Virulence is defined by…

A

The relative CAPACITY of a microbe to cause damage in a host

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20
Q

Disease outcomes is a function of (BLANK) & (BLANK)

A

Bacterial virulence factors and host defense factors

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21
Q

Secreted effectors

A

Co-opt host cell signalling pathways

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22
Q

Pathogenicity Islands (PAIs)

A

Chromosomal loci encoding multiple virulence factors

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23
Q

Virulence factors can be encoded on what 3 genetic elements

A
  1. bacterial chromosomes
  2. plasmids
  3. lysogenic bacteriophage
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24
Q

(BLANK) is a major barrier of infection

A

The mucus layer (i.e. epithelial cells)

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25
Q

Mucin contains…

A

Sialic acid and sulfated polysaccharides

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26
Q

Goblet cells

A

Excrete mucus

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27
Q

The ECM consists of proteins embedded in (BLANK) & (BLANK)

A

Sugar and proteoglycans

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28
Q

The most abundant protein in the ECM

A

Collagen

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29
Q

Connects integrin proteins to ECM

A

Fibronectin

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30
Q

Lamanin binding protein

A

protein used by pathogen to bind to ECM

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31
Q

Hyaluronidase

A

A mucinase (degrades mucin)

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32
Q

Coagulase

A

Forms fibrin blood clots

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33
Q

Plasmin

A

Degrades fibrin blood clots

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34
Q

Streptokinase & staphylokinase are…

A

Plasminogen activators

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35
Q

PAI1 & PAI2 are bound to…

A

Vitronectin

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36
Q

Plasmin activate

A

Marix Metallo Proteinases (MMPs)

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37
Q

MMPs convert (BLANK) into (BLANK)

A

Procollagenase into collagenase

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38
Q

Sortases

A

Catalyze attachment of adhesins in GPB

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39
Q

Cell wall sorting signal (CWSS)

A

Protein recognized by sortase

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40
Q

Leukocidins & hemolysins are…

A

Pore forming exotoxins

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41
Q

Cytolytic toxins cause…

A

Swelling and cell lysis

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42
Q

Phospholipases can cause…

A

Gas gangrene

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43
Q

Gas gangrene is disease resulting from…

A

Clostridium perfringens

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44
Q

A-B subunits are first (BLANK) & then (BLANK)

A

Endocytosized, dissociate

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45
Q

A-B toxins function by…

A

bARTTs (ADP ribosilation); inactivating target proteins

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46
Q

Superantigens stimulate…

A

T cell; cyctokine release

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47
Q

Lipis A is the toxic part of…

A

LPS in GNB

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48
Q

Roup LPS (LOS)

A

Lacks the O antigen

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49
Q

O antigen blocks…

A

Omptins (bacterial surface proteins)

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50
Q

Bacteria scavenge for (BLANK) and convert to (BLANK)

A

Fe3+, FE2+

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51
Q

3 host proteins that bind Fe are…

A

Hemoglobin, lactoferrin, and transferrin

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52
Q

Genes that regulate Fe dissociation from heme

A

Iron regulated surface determinant pathway (isd)

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53
Q

FUR

A

Fe-binding respressor regulated siderophore gene transcription

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54
Q

2 mechanisms of survival for bacteria in pathogen containing vacuoles

A
  1. block phagosome acidification

2. prevent phagosome-lysosome fusion

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55
Q

Rho GTPase INACTIVATION results in…

A

Actin depolymerization

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56
Q

Rho GTPase ACTIVATION result in…

A

Actin Polymerization

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57
Q

Capsules are composed of…

A

Sugars and amino acids from host

58
Q

Complement-mediated lysis results from pore forming (BLANK)

A

Menmbrane Attack Complex (MACs)

59
Q

A component of the host ECM that blocks formation of MACs

A

Vitronectin

60
Q

Serum resistance

A

Ability of pathogen to block complement mediated lysis (co-opts host factors)

61
Q

C4BP, Factor H, FHL-1

A

Block proteolysis cascade

62
Q

Caspases are proteases with (BLANK) residues that cleave after (BLANK) residues

A

Cysteine, aspartic acid

63
Q

Neutrophiles secrete DNA and proteins to create…

A

Neutrophile extracellular Traps (NETs)

64
Q

C5a peptidase

A

Blocks complement

65
Q

IgG proteases

A

Degrade antibodies

66
Q

s-IgA proteases

A

Breaks down IgA dimer in mucous layer

67
Q

4 clinically relevant GPC (by genus)

A
  1. Streptococcus
  2. Enterococcus
  3. Staphylococcus
  4. Micrococcus
68
Q

2 Catalase Negative GPC

A

Streptococcus, enterococcus

69
Q

2 Catalase Positive GPC

A

Staphylococcus, Micrococcus

70
Q

Streptococcus and micrococcus colonies are characteristically…

A

small, translucent, chains

71
Q

Staphylococcus and micrococcus colonies are characteristically…

A

larger, opaque, clusters

72
Q

Lancefield groupings refer to differences in…

A

Antigenic expression in C carbohydrate (inhibits lysozyme)

73
Q

GAS

A

Group A Streptococcus

74
Q

GABHS

A

Group A beta hemolytic streptococcus

75
Q

What ordering of traits would help characterize streptococci

A
  1. size
  2. hemolytic pattern
  3. catalase
76
Q

Beta hemolysis is (BLANK), resulting from (BLANK)

A

Complete hemolysis, streptolysin S and O

77
Q

Streptolysin S is oxygen- (BLANK) and (BLANK)

A

stable, cytolytic

78
Q

Streptolysin O is oxygen- (BLANK) and (BLANK)

A

labile, apoptotic

79
Q

Alpha hemolysis is (BLANK), resulting from (BLANK)

A

Partial hemolysis, bacterial hydrogen peroxide oxidizing Fe 2+ to Fe3+ (e.g. hemoglobin to methylglobin)

80
Q

Pharyngitis, etiological agent…

A

Streptococcus pyogenes, throat

81
Q

Neonatal sepsis, etiological agent…

A

Streptococcus agalactiae

82
Q

Pneumonia, etiological agent…

A

Streptococcus pneumoniae

83
Q

Nosocomial UTI, etiological agent…

A

Enterococcus faecalis

84
Q

Dental plaques, etiological agent…

A

Streptococcus mutans (i.e. viridans)

85
Q

Severely invasive GAS serotype…

86
Q

What causes necrotizing faciitis in invasive GAS

A

Streptococcal Toxic Shock Syndrome (STSS), exotoxin A

87
Q

How does Sequelae disease casue host damage

A

The host immune reaction to GAS M proteins (cross reaction)

  1. cross reacts with myosin in heart valves leading to Acute Rheumatic Fever (ARF)
  2. antibody complexes build up leading to kidney failure (acute glomerulonephritis)
88
Q

GAS mechanisms of colonization…

A

Adherence- fimbrial/non-fimbrial
Quorum sensing in biofilms
Nutritional adaptation through transcriptional regulation
Host modulation

89
Q

3 events that occur from GAS colonization/manipulation…

A

Internalization, Cytokine release, Apoptosis

90
Q

How does GAS colonize multiple sites in host

A

Expresses multiple adhesins (attached using sortase)

91
Q

3 adhesins (and their binding substrate) found in GAS

A 
M proteins (components of the ECM, Fn)
Ig-binding proteins (antibodies)
Protein F (binds Fn)
92
Q

The (BLANK) that coats GAS allows the pathogen to evade host immune response

A

Hyaluronic acid capsule

93
Q

Streptodornase

A

DNAase used by GAS to to destroy NETs

94
Q

How does GAS evade opsonophagocytosis

A

M protein binding to Fn and IgG proteases (IdeS)

95
Q

SIC in GAS inhibits…

A

complement and therefore MAC formation

96
Q

Exotoxin A

A

Pyrogenic (fever inducing) superantigen

97
Q

Exotoxin B

98
Q

Exotoxin C

A

Superantigen

99
Q

Streptolysin O

A

Pore forming cytolytic (apoptosis in phagocytes)

100
Q

SLS

A

AKA streptolysin S is a membrane disrupting cytolytic (destruction of tissue/cells)

101
Q

SLS is in the (BLANK) family of exotoxins and contains multiple modified (BLANK,BLANK, and BLANK) amino acids

A

TOMMS

Cys, Ser, Thr

102
Q

The (BLANK) operon for SLS contains what 3 components

A

Sag

sagA gene, modifying enzymes, and ABC transporter

103
Q

What is essential for the bioactivity of SLS

A

Residue modifications that result in a more rigid structure

104
Q

What two enzymes are responsible for SLS residue modifications

A

SagC (cyclodehydratase) and SagB (dehydrogenase)

105
Q

SLS modification is a (BLANK) process

A

heterocyclic

106
Q

SLS residue serine is converted to (BLANK)

107
Q

SLS residue threonine is converted to (BLANK)

A

Methyloxazole

108
Q

SLS residue cyteine is converted to (BLANK)

109
Q

Name two virulent factors specific to GAS M1T1

A

bacteriophage-encoded streptodornase D and exotoxin A

110
Q

Mutations in (BLANK) cause M1T1 invasive disease

A

CovRS (two component system, AKA TCS)

111
Q

CovS is a…

A

Sensor kinase that phosphorylates CovR

112
Q

CovR is a…

A

Response regulator that NEGATIVELY regulates virulence genes

113
Q

Inactivation on CovS or CovR leads to (BLANK) and (BLANK)

A

Up regulation of virulence factors and down regulation of exotoxin B

114
Q

Example of GBS…

A

Streptococcus agalactiae

115
Q

GBS virulence factors…

A

Capsule, proteases, and hemolysins

116
Q

Viridans Streptococci can cause…

A

Dental caries and bacterial endocarditis (sub-acute)

117
Q

Viridans Streptococci are (BLANK) hemolytic

A

Alpha, partial hemolysis

118
Q

How to differentiate Streptococcus pneumoniae by shape…

A

It is a football-shaped diplococci

119
Q

Streptococcus pneumoniae can cause…

A

Otis media, meningitis, and pneumococcal pneumoniae

120
Q

Pneumococcal pneumoniae is usually (BLANK) and produces (BALNK) sputum

A

Community acquires (CA), rust colored

121
Q

S. pneumoniae virulence factors against mucus layer are…

A

capsule (ESSENTIAL), exoglycosidases, pneumolysin

122
Q

Pneumocin

A

A bacteriocin in S. pneumoniae active against other streptococcus

123
Q

Pneumolysin

A

Pore forming cytolytic toxin that decrease ciliary beating in lungs

124
Q

List 3 host barriers to S. pneumoniae adherence in nasopharyx are…

A
  1. mucus layer
  2. lysozyme
  3. s-IgA
125
Q

Exoglycosidases

A

deglycosylate mucus glycocojugates (decreases mucus viscosity)

126
Q

S. pneumoniae virulance factors against lysozyme are…

A

Secretes deacetylases that make it resistant to lysozyme recognition

127
Q

S. Pneumoniae virulence factors against s-IgA are…

A

Secretes s-IgA proteases that prevent bronchial ciliary escalator

128
Q

Formerly group D Streptococcus

A

Enterococcus faecalis

129
Q

Norma microbiota in GI tract are…

A

Enterococcus faecium

130
Q

Vacomycin resistant enterococci (VRE) are most likely to result from (BLANK) infections

A

Nosocomial

131
Q

Enterococcus can cause (BLANK) UTIs that move from the (BLANK) to the (BLANK)

A

Ascending, urethra, kidneys

132
Q

If a strep test came back POSITIVE the results indicate it’s (BLANK) and you should (BLANK)

A

GAS, treat with antibiotics

133
Q

If a strep test came back NEGATIVE the results indicate it’s not (BLANK) and you should (BLANK)

A

GAS, test hemolysis (Inoculate BAP)

134
Q

If GBS were tested for CAMP factor using a CAMP test the result would show…

A

a synergistic hemolytic effect between GBS and S. aureus

135
Q

S. pneumoniae can be identified using a (BLANK) test which would result in (BLANK)

A

Quellung, capsular swelling

136
Q

Epithelial and endothelial cells are connected to neighboring cells by blank and blank

A

TJs and AJs

137
Q

Occulin, zonulin, and ZO-1 are examples of…

A

TJ PROTEINS

138
Q

Cadherins are examples of…

A

AJ proteins

139
Q

Disrupting the cell junctions increases blank

A

Paracellular permeability

140
Q

Cells are connected to the ECM through blank and blank

A

Focal adhesions and hemidesmosomes

141
Q

Endotoxins bind to LPS binding protein and the complex binds to blank and blank proteins on macrophage

A

CD14 and TLR4

142
Q

When endotoxin activates host proteins this induces high concentrations of blank and blank which activates coagulation cascade and immune system response

A

Cytokines and ROS

Clinical Micro (4 decks)

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