Bacterial Structures Flashcards

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1
Q

Al bacterial cells must possess

A

cell membrane, genome, ribosomes, intracellular macromolecules, almost always a cell wall

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2
Q

Extrachromosomal elements (ECE)

A

plasmids or prophages may be present

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3
Q

Describe a bacterial ribosome

A

70S (50S + 30S)

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4
Q

What are 3 cell surface structures that may or may not be present on bacteria

A

Flagella, Pili, Capsules

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5
Q

dipococci

A

pair of cocci

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6
Q

streptococci

A

chain of cocci

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7
Q

staphylococci

A

cluster of cocci

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8
Q

antimicrobics may alter

A

cell morphology (shape and arrangement)

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9
Q

Flagella or antigen ____

A

H

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10
Q

Flagella is composed of

A

polypeptides - different than pili

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11
Q

Plain flagella

A

extend from the cell surface into the environment for motility

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12
Q

Endoflagella of spirochetes

A

internal structure that allow them to perform a corkscrew movement

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13
Q

Flagella function to

A

provide motility in liquid and some surface translocation

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14
Q

What allows flagella to propel?

A

sensory system control via chemotaxis

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15
Q

Virulence factor of flagella

A

motility with chemotaxis

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16
Q

H-antigen

A

flagella

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17
Q

Pili are composed of

A

polypeptide chain - different than flagella

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18
Q

Normal pili and sex pili

A

extend out from the cell surface into the environment

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19
Q

Pili functions to

A

aid in adherence to host, antiphagocytic, involved in surface translocation (pili type IV)

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20
Q

Sex pilus function

A

conjugation (spread of antibiotic resistance)

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21
Q

Another name for capsules

A

glycocalyx, exopolysaccharide (EPS), slime layer

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22
Q

Capsule is composed of

A

complex polysaccharides, simple sugar, or D-glutamic acid

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23
Q

O antigen

A

LPS

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24
Q

K antigen

A

capsule formed from simple sugar, complex polysaccharide, or D-glutamic acid

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25
Q

Biofilm

A

complex, 3-D structure, microcolony of bacteria or yeast, enmeshed in a mucoid exopolysaccharide film

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26
Q

Biofilm composition

A

exopolysaccharides and in some cases proteins (amyloid fibers)

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27
Q

Phenotypic changes of bacteria in biofilms

A

non-motile, persist even with antimicrobials, multi-drug resistant

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28
Q

the activation of biofilm formation involves

A

quorum sensing: sensing the density of the population and switching gene expression

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29
Q

Re-seeding from biofilm

A

some cells in the biofilm revert back to normal, therefore even if anti-microbials have been used the infection may return

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30
Q

How are cells released from a biofilm and when?

A

when the amyloid structural protein is broken down by D-A.A. when the situation dictates it

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31
Q

Biofilms function

A

adherence to host tissue and surfaces (surface colonization), protection against antibiotics and desiccation (Drying out)

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32
Q

surface colonization of biofilms allow them to

A

thrive in a moving environment

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33
Q

K antigen

A

capsular antigen

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34
Q

O antigen

A

LPS

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35
Q

Do gram positive bacteria have capsules?

A

They may or may NOT have capsules

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36
Q

Do gram negative bacteria have capsules?

A

They may or may NOT, O antigen + and K antigen - if no capsule, O antigen + and K antigen + is capsule differs from LPS, O antigen + and K antigen - if capsule is an extension of LPS

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37
Q

S-Layers

A

layer lying directly on cell walls, rigid layer with pores of fixed diameter

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38
Q

S-Layers are composed of

A

protein or glycoprotein

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39
Q

S-Layers function

A

resistance to C3b binding (resists complement mediated killing), prevents phagocytosis by PMNs

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40
Q

Translocation

A

passage through human cells to access new sites

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41
Q

Genera capable of Translocation

A

H. flu, S. pyrogenes, M. tuberculosis

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42
Q

Paracellular translocation

A

passage between cells to enter tissues

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43
Q

The ability to slide on solid surfaces is associated with

A

biofilm formation at least with Mycobacterium smegmatis

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44
Q

Polypeptides embedded in the lipid bilayer are stabilized by

A

divalent cations (Ca and Mg) and hydrophobic interactions with fatty acid moiety of phospholipids

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45
Q

Which genera of bacteria DO CONTAIN sterols?

A

Mycoplasma, helicobacter, ehrlichia, Anaplasma spp.

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46
Q

Cell membrane characteristics

A

permeable for transport, specific transport mechanisms for secretion of proteins (6 types), respiratory components, biosynthetic pathways, sensory and osmoregulatory mechanisms and chemotaxis

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47
Q

Type III transport system (injectosomes)

A

conserved multiprotein system that pathogenic gram-NEGATIVE bacteria use to insert protein toxins into cells

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48
Q

Respiratory components found in the cell membrane

A

ETC, ATP synthase, generating proton motive force

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49
Q

Cell membrane contains components for biosynthesis of

A

cell wall, cellular replication (septal ring)

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50
Q

The cell wall regulates osmotic pressure, such that the bacterial cell is ____________ compared to the environment

A

hypertonic

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51
Q

Chemotaxis mechanisms lie within the

A

cell membrane

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52
Q

The peptidoglycan layer in the gram positive cell wall is much ______ than the gram negative cell wall

A

thicker

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53
Q

Describe the peptidoglycan layer of the cell wall of gram-positive cells

A

thick peptidoglycan layer, covalently linked polysaccharides, lipoteichoic acid extend through the peptidoglycan layer, no outer LPS layer

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54
Q

Describe the peptidoglycan layer of the cell wall of gram-negative cells

A

thin peptidoglycan layer, no covantely linked polysaccharides or LA extending through, contains an outer layer of LPS, located within the periplasm

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55
Q

Cell wall function

A

maintain cell shape, shield from environment, virulence and toxicity factors

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56
Q

What portion of the cell wall is important in maintaining cell shape and providing mechanical strength

A

peptidoglycan layer

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57
Q

What portion of the cell wall determines the gram staining

A

peptidoglycan layer

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58
Q

Peptidoglycan layer composition

A

woven network of NAG and NAM (N-acetylmuramic acid and N-acetylglucosamine)

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59
Q

Lysozyme

A

cleaves the amino sugar bonds (NAM, NAG) of the peptidoglycan layer, lysing the bacteria

60
Q

Where is lysozyme found

A

saliva and tears

61
Q

Peptide stems allow for

A

(amino acid side chains) weaving/covalent linking of the NAM and NAG molecules of the peptidoglycan layer

62
Q

Peptide side chains of NAM and NAG must contain

A

D-A.A.

63
Q

Peptidoglycan layer functions

A

prevents cell bursting from osmotic forces, gives cell shape

64
Q

Which bacteria lack peptidoglycan

A

Mycoplasma, Rickettsia, Ehrlichia, Anaplasma

65
Q

Outer cell membrane is

A

a lipid bilayer with phospholipid as the inner leaflet and LPS as the outer leaflet

66
Q

Periplasm

A

found outside the cell membrane of gram negative bacteria and contains the peptidoglycan layer

67
Q

Periplasm function

A
  1. OSMOTIC PROTECTION

nutrient uptake from OM to CM, chemotaxis, degradative enzymes, osmoregulation

68
Q

Are Gram-negative bacterium more or less susceptible to cell-wall active agents?

A

less; only 1 layer of peptidoglycan which is hidden in the periplasm beneath the outer membrane

69
Q

Outer Membrane functions

A
  1. SHIELDS AGAINST ENVIRONMENTAL CHANGES,
    virulence and toxicity factors, antigenic components, receptors for antibodies and sex pilus, anchors external structures of bacteria
70
Q

Outer Membrane prevents entrance of

A

dyes, detergents, hydrolytic enzymes (lysozome)

71
Q

Outer membrane composition

A

lipopolysaccharide, phospholipid, proteins

72
Q

The outer leaflet of the outer membrane lipid bilayer

A

LPS

73
Q

The inner leaflet of the outer membrane lipid bilayer

A

phospholipid

74
Q

Porins

A

Outer membrane proteins that form aqueous channels to allow hydrophilic substances pass through the OM

75
Q

LPS constituents

A

Lipid A + core + O-antigenic chain

76
Q

Lipid A is composed of

A

fatty acid + disaccharide, phosphate groups, fatty acids, LPS toxicity is associated with Lipid A

77
Q

Core is composed of

A

oligosaccharides, sugars, ketodeoxyoctulonate [KDO] - common in enteric bacteria

78
Q

Terminal Polysaccharide

A

O antigen

79
Q

Terminal Polysaccharide is composed of

A

sugars, a unit repeating, highly specific and highly variable

80
Q

Terminal polysaccharide variation

A

each strain of bacteria possesses a chemically distinct O-antigen

81
Q

Lipooligosaccharide (LOS) is composed of

A

Lipid A + extended core

82
Q

Lipooligosaccharide (LOS) is

A

synthesized in place of LPS in Neisseriameningitidis and N. gonorrhoeae, and H. flu and H. ducreyi

83
Q

Lipooligosaccharide (LOS)

A

lacks O-antienic chain

84
Q

LPS functions

A

structural component of OM, pyrogen, complement pathway, hageman factor, release of endogenous mediators

85
Q

LPS acts as a pyrogen by producing

A

induction of IL-1 which acts on the hypothalamus, or DIRECTLY acting on the hypothalamus

86
Q

LPS activates __________ complement pathway

A

alternative

87
Q

LPS activates ___________ factor

A

Hageman (factor XII)

88
Q

LPS induces the release of endogenous mediators:

A

TNF-alpha, IL-1, IL-6, arachidonic metabolites, bradykinin, histamines, NO, free radicals

89
Q

LPS structure is

A

heat stable unless with strong oxidizers

90
Q

LPS does not form

A

toxoids, due to to heat stability

91
Q

How would one detoxify LPS?

A

burning or oxidation

92
Q

LPS may potentially cause

A

SIRS; with macrophages, PMNs, and endothelial cells as effector cells

93
Q

Bacterial endospore-formers

A

Clostridium and Bacillus

94
Q

Activation of the SIRS pathway occurs via

A

infection (esp gram-negative bacteria) or non-infectious etiology

95
Q

How does LPS activate SIRS immune response

A

LPS binds LBP, LBP-LPS complex binds membrane-bound CD14 on PMNs, macrophages, and monocytes to and activates TLR; complex interacts with soluble CD14 which causes endothelial leakiness (hypotension, edema)

96
Q

ARDS (acute respiratory distress syndrome) is a common feature of _________, not _________

A

distributive shock, not systemic inflammatory response syndrome

97
Q

Endogenous mediators released by activation of TLR result in

A

temperature > 38 or < 36
HR >90
RR >20
Leukocytosis >12,000 or leukopenia <4000

98
Q

The clinical definition of SIRS is

A
TWO or MORE symptoms:
temperature > 38 or < 36
HR >90
RR >20
Leukocytosis >12,000 or leukopenia <4000
99
Q

SIRS consists of

A

ONE or MORE
Systemic inflammation/ “hyperinflammatory state”
Activation of coagulation
Inhibition of fibrinolysis

100
Q

Why does activation of coagulation occur in SIRS?

A

LPS activation of Hageman Factor XII, activates clotting system and fibrinolysis, followed by inhibition of fibrinolysis by plasminogen activator inhibitor

101
Q

plasminogen activator inhibitor

A

causes inhibition of fibrinolysis during SIRS

102
Q

DIC Disseminated Intravascular Coagulation

A

results from accumulation of undissolved thrombin in the microcirculation

103
Q

DIC may lead to

A

multi organ failure and purpuric skin lesions

104
Q

Survival of the hyper inflammatory state is followed by

A

hypo inflammatory state “immunoparalysis”

105
Q

Hypoinflammatory state is manifested by

A

loss of delayed hypersensitivity
failure to clear primary infection
development of secondary infection
reactivated dormant viruses

106
Q

Sepsis is defined by

A

the presence of BOTH:

  • A proven infection
  • Presence of 2 or more SIRS manifestations
107
Q

Severe sepsis is defined by

A

the presence of BOTH:

  • Sepsis
  • Organ Failure
108
Q

Septic Shock is defined by

A

the presence of BOTH:

  • Severe sepsis
  • refractory hypotension (40-50/30-40)
109
Q

Shock is defined by

A

inadequate perfusion of tissues

110
Q

3 Types of shock

A

cardiogenic, vascular obstructive, hypovolemic

111
Q

Distributive shock is a type of

A

hypovolemic shock

112
Q

Distributive shock consists of

A

endothelial cell dysfunction (leakiness), loss of vascular resistance –> hypotension, coagulopathy/DIC, septic cardiomyopathy –> reduced CO (reversible)

113
Q

Septic cardiomyopathy is induced by

A

LPS, C5A, IL-1beta, TNF-alpha, IL-6

114
Q

Clinical manifestations of distributive shock

A

fever or hypothermia, chills, leukopenia or leukocytosis, high HR and RR, DIC, hypotension shock and DIC can lead to MOF or MOD

115
Q

Therapy for early Sepsis - sepsis resuscitation bundle

A

Measure serum lactate, obtain blood specimen for culture, administer broad-spectrum antibiotics, if hypotensive administer fluids or vasopressin, achieve O2 saturation

116
Q

Therapy for early Sepsis - sepsis management bundle

A

corticosteroids, tight glycemic control

117
Q

Failed sepsis therapies

A

anti-TLR4 (eritoran tatrasodium) and drotecogin alfa (activated, recombinant protein C)

118
Q

Detecting LPS in pharmaceutical industry

A

Limulus amebocyte lysate test, mAb anti-LPS

119
Q

endotoxin v exotoxin - chromosome encoded?

A

endotoxin only chromosome encoded, exotoxin may be encoded by chromosome or plasmid

120
Q

endotoxin v exotoxin - required for survival?

A

endotoxin - yes; exotoxin - no

121
Q

endotoxin v exotoxin - composition?

A

endotoxin - sugar-phosphate-fatty acids

exotoxin - protein

122
Q

endotoxin v exotoxin - number encoded by bacteria?

A

endotoxin - more than 1 structural form

exotoxin - one specific form

123
Q

endotoxin v exotoxin - toxoid?

A

endotoxin - NO, heat stable

exotoxin - YES, heat labile

124
Q

endotoxin v exotoxin - receptor?

A

endotoxin - general PAR receptor

exotoxin - specific toxin receptor

125
Q

endotoxin v exotoxin - mechanism?

A

endotoxin - systemic reaction > SIRS > DS

exotoxin - host cell reaction of altered function, lysis, molecule mimicry

126
Q

endotoxin v exotoxin - pyrogens

A

endotoxin - exogenous (direct through BBB) and endogenous pyrogen (IL-1, TNF-alpha)
exotoxin - no

127
Q

endotoxin v exotoxin - presence in human blood

A

endotoxin - sepsis

exotoxin - toxemia

128
Q

name the main components of the gram-positive cell wall

A

peptidoglycan, teichoic acid, lipoteichoic acid (in outer CM leaflet)

129
Q

Peptidoglycan in gram positive bacteria

A

extensively cross-linked (muramic side chains) and present in large amounts

130
Q

Lipoteichoic acid structure

A

glycerol-PO4 or ribitol-PO4 covalently linked to glycolipid, noncovalently linked to outer leaflet of CM, extending through the peptidoglycan to the external environment

131
Q

What is the primary factor in the adhesion of Strep pyrogenes to fibronectin on pharyngeal epithelial cells

A

Lipoteichoic acid

132
Q

Teichoic acid structure

A

glycerol-PO4 or ribitol-PO4 covalently linked to peptidoglycan, extending through the peptidoglycan to the external environment

133
Q

Teichoic acids medical importance

A

peptidoglycan + teichoic acid can produce endotoxin-like shock in patients with staph. aureus by interacting with C-reactive protein and activating the alternative complement pathway

134
Q

How can DIC and DS occur with pathogens lacking LPS?

A

PARS recognition of PAMPS, releasing endogenous mediators that cause SIRS

135
Q

NOD1 and NOD2

A

internal PAR, NOD2 deficiency is related to Crohn’s

136
Q

TLR

A

extracellular PAR, bind peptidoglycan, teichoic acid, N-f-met-leu-phe, CpG, LPS

137
Q

Spores

A

a complete but inactive cell in a protective shell, forms inside mother cell which dies

138
Q

Most bacteria __________ form spores

A

DO NOT

139
Q

Spores are formed in order for bacteria to

A

survive adverse conditions until environmental conditions are favorable

140
Q

bacterial endospores have increased

A

longevity, resistance to heat/temp, resistance to desiccation, resistance to chemical agent

141
Q

What 2 genera of bacteria are spore-forming

A

bacillus and clostridium

142
Q

Small colony variants

A

growth-deficient variants that fem colonies, due in part to deficiencies in energy metabolism, possess enhances resistance to antibiotics, recurrent infections

143
Q

small colony variants are formed by

A

Staphylococcus aureus, pseudomonas aeruginosa, E. coli and UTIs

144
Q

Small colony variants are associated with chronic, recurrent infections of

A

heart,lung, bones, urinary tract

145
Q

Biofilm and SCV are phenotypic switching, meaning

A

they can revert back to their previous form and re-seed