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GMS6121 - Infectious Diseases > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

bacteria morphology

A

coccus
bacillus (rod)
spirochete
vibrios, filamentous, coccobacilli

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2
Q

what is cell wall

A

rigid structure surrounding the cell membrane

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3
Q

cell wall functions

A

prevent osmotic lysis
protect cell from external stresses (host)
contributes to virulence
target for antimicrobials

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4
Q

what makes a bacteria gram pos

A

no outer mem
thick peptidoglycan
looks blue when stained

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5
Q

what makes a bacteria gram neg

A

outer membrane w an inner (thinner) layer of peptidoglycan
looks pink when stained

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6
Q

what makes a bacteria acid-fast

A

have waxes and fatty acids on the outside of peptidoglycan
hydrophobic components difficult to stain, but once stained it retains stain
red on blue

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7
Q

what is the most common acid fast bacteria

A

Mycobacteria
(TB)

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8
Q

what are the main mycobacterial virulence factors

A

mycobacteria are acid-fast
mycolic acid, Wax D, cord factor, arabinogalactans, and sulfolipids

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9
Q

wall less bacteria stain

A

need special stain
sensitive to stress

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10
Q

features of gram pos bacteria

A

thick peptidoglycan wall (chain link fence)
resist lysis by complement, but still can be opsonized
teichoic acids and lipoteichoic acids
other proteins and carbohydrates (fibrillar layer, carbohydrate capsule)

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11
Q

teichoic acid

A

gram pos
Ribitol or glycerol phosphate + side chains
Involved in virulence and Ag classification

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12
Q

features of gram neg bacteria

A

outer membrane (2nd lipid bilayer)
periplasmic space between inner and outer membranes
single layer of peptidoglycan in periplasmic space
porins enable diffusion across outer mem
LPS for pathogenesis

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13
Q

what are polymyxins

A

work on outer mem (gram neg), work as cationic detergents
can target LPS

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14
Q

LPS features

A

endotoxin for gram neg
MOST HIGHLY CONSERVED PORTION OF LPS = LIPID A
made up of lipid A and core oligosaccarides
Lipid A has endotoxin activity, beta-hydroxy myristic acid, phosphastes, and glucosamines
core is highly conserved among different bacteria
recognized by TLR4

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15
Q

what does TLR4 recognize

A

LPS

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16
Q

what is beta-hydroxy myrisitc acid

A

a unique C14 fatty acid
part of lipid A in LPS

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17
Q

smooth vs rough LPS

A

rough = core + lipid A
Smooth = rough + O Ag

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18
Q

what is O Ag

A

repeating sugar units on smooth (not rough) LPS
Antigenic and highly variable amount species and strains

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19
Q

what is LOS

A

LPS without O Ag
(it ‘lost’ the O –> LOS)

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20
Q

what is the most common wall less bacteria

A

mycoplasma

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21
Q

features of wall-less bacteria

A

No cell wall (no peptidoglycan)
No outer membrane
Incorporation of CHOLESTEROL from host (toughens mem)
Very labile
No definite shape
Small genome

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22
Q

features of peptidoglycan

A

unique to prokaryotes
lysozyme hydrolyses (breaks down) backbone
composition: N-acetyl glucosamine - N-acetyl muramic acid
pentapeptide with L and D amino acids

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23
Q

what do beta lactams target

A

inhibit transpeptidation (D-ala-D-ala) of peptidoglycan
How?
Transpeptidase enzymes that cross link can recog penicillin instead of D-ala-D-ala > inactivates transpeptidase enzymes > no cross linking
bactericidal

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24
Q

name the beta lactams

A

penicillins (ampicillin and methicillin) and cephalosporins
Target peptidoglycan

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25
Q

what does vancomycin target

A

transpeptidation and transport (binds to D-Ala-D-Ala, note difference with beta-lactams)
TOO BIG, DOES NOT WORK ON GRAM NEG

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26
Q

what does bacitracin target

A

lipid carriers, transport of peptidoglycan subunits across mem
TOO BIG, DOES NOT WORK ON GRAM NEG

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27
Q

beta lactams vs vancomycin

A

beta lactams: target transpeptidase enzymes
vancomycin: target D-ala-D-ala

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28
Q

what is the difference between gram pos and gram neg peptidoglycan

A

gram pos: L-lys-(gly)5-D-ala
gram neg: DAP-D-ala
(DAP acts as lysine in gram neg)

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29
Q

peptidoglycan synthesis

A

transport through cytoplasmic membrane
(bacitracin-sensitive)
polymerize backbone
cross-link peptides
third amino acid - NH2 side chain (lysine [gram- positives] or DAP [gram-negatives]) peptide bond displaces terminal amino acid (D- alanine) of adjacent peptide chain, crosslinking chains and conferring rigidity

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30
Q

penicillin binding proteins (PBPs)

A

perform crosslinking of peptidoglycans

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31
Q

pentaglycine bridge

A

extends from lysine to form cross-links in peptidoglycan

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32
Q

muramyl dipeptide

A

part of peptidoglycan backbone
N-acetyl glucosamine and N-acetyle muramic acid w two aa’s haning down
HIGHLY INFLAMMATORY
recog by TLR2

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33
Q

what does TLR2 recognize

A

muramyl dipeptide (part of peptidoglycan layer)

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34
Q

bacteria capsule

A

aka slime layer or K Ag
not impermeable
Both gram pos and gram neg can make
made of polysaccharides
important for virulence : inhibits complement and phagocytosis

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35
Q

what is glycocalyx

A

extracellular polysaccharide important for biofilms

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36
Q

flagella

A

aka H antigen
propeller
motility and chemotaxis
recognized by TLR5

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37
Q

what does TLR5 recognize

A

flagella

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38
Q

Pili/fimbriae

A

2 diff types: adherence and genetic exchange, some do one or the other, some do both

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39
Q

fibrillar layer

A

fuzzy protein coat on surface
virulence

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40
Q

bacterial spores

A

certain gram pos only - both aerobic and anaerobic
metabolically inactive
resistant to heat (boiling), desiccation
contain dipicolinic acid

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41
Q

vegetative state in bacteria

A

growing

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42
Q

germination in bacteria

A

spore goes to vegetative (growing) state

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43
Q

sporulation in bacteria

A

vegetative makes spores in response to stress

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44
Q

bacterial cytoplasmic mem functs

A

ONLY INTACT LIPID BILAYER
transport: facilitated diffusion, active transport, group translocation (phosphotransferase – carbos)
electron transport and oxidative phosphorylation
energy production
motility
replication (no actin or MTs, used to separate chromosomes

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45
Q

what is group translocation

A

phosphotransferase used to move carbs, phosphorylation of carb to transport it

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46
Q

nucleoid

A

Single, circular structure (haploid genome) –> mutations result in dominant phenotype
Not in nucleus - no nuclear mem, Transcription in cytoplasm w translation
Supercoiling - DNA gyrase –> important for DNA replication, can store energy

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47
Q

what do quinolones target

A

gyrase (supercoiling) and DNA rep

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48
Q

name the quinolones

A

nalidixic acid

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49
Q

what does metronidazole target

A

incorporated into DNA after reduction by anaerobes, inhibiting DNA replication

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50
Q

fermentation v respiration

A

fermentation = organic e- receptor
respiration = inorganic e- receptor

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51
Q

obligate aerobes

A

require oxygen

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52
Q

facultative anaerobes

A

grew well in presence or absence of oxygen

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53
Q

microaerophilic

A

prefer low oxygen

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54
Q

aerotolerant

A

tolerate low amounts of oxygen

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55
Q

obligate anerobes

A

cannot tolerate oxygen

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56
Q

siderophores

A

high affinity for Fe, take the Fe from host to use for replication
important for virulence

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57
Q

folic acid metabolism

A

humans need to consume it, bacteria need to synthesize it
THFA acts as a C donor, then becomes DHFA, needs to be recycled

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58
Q

what does trimethoprim target

A

inhibits dihydrofolate reductase
folic acid recycling
blocksconvertion of DHFA back to THFA
technically also affects humans but much more severe for bacteria

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59
Q

what does sulfonamide target

A

blocks folic acid
acts as a PABA analog that inhibits dihydropteroate synthetase (not in humans, needed for folic acid metabolism)

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60
Q

bacterial RNA polymerase

A

Alpha-alpha-beta-beta’ is core, has enzymatic activity
also need sigma to binds to promoters, but the pol is technically just the core

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61
Q

what is bacterial holoenzyme

A

alpha-alpha-beta-beta’ core + sigma

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62
Q

what does rifampin target

A

RNA synthesis (beta subunit of RNA pol core)

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63
Q

Factor independent vs Rho dependent transcription

A

factor independent - default
rho dependent - RNA pol needs additional subunit for transcription

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64
Q

how is transcription regulated in bacteria

A

initiation is regulated
once transcription starts, it just goes

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65
Q

polycistronic operons

A

several genes transcribed from same promoter and regulated by the same conditions

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66
Q

lac operon

A

Absence of lactose: Lac I binds operator (o, between promoter (p) and gene), prevents Pol from transcribing > no transcription
Lactose present: inducer (allolactose/lactose/IPTG) binds Lac I, prevents Lac I from inhibiting operator, Pol functs
RNA POL CAN BIND PROMOTER IN BOTH, LAC I JUST BLOCKS IT BY BINDING O
needs 2nd signal from CAP+cAMP

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67
Q

quorum sensing

A

important in biofilms
small inducer molecules secreted
when conc reaches threshold (quorum has been attained) > gene expression changes

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68
Q

what is the main difference between transcription and translation in humans v bacteria

A

bacteria = co-transcription-translation
no mem, no nucleus, both happen at same time in cytoplasm

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69
Q

what do aminoglycosides target

A

ribosome (translation)

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70
Q

name to the aminoglycosides

A

streptomycin, kanamycin, gentamicin, neomycin
(target ribosome)

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71
Q

what does tetracyclines target

A

ribosome (translation)
bacteriostatic

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72
Q

what does chloramphenicol target

A

ribosome (translation)

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73
Q

what does macrolides target

A

ribosome (translation)

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74
Q

name the macrolides

A

erythromycin and azithromycin
(target ribosome)

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75
Q

where can protein localize to

A

Cytosol (Cytoplasm), Cell mem, Periplasm (gram-neg), Outer mem (gram-neg), Extracellular, Inside host cells

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76
Q

what pathways mediated secretion in bacteria

A

Primary = Sec pathway (uses N terminal hydrophobic leader seq) Secondary = Tat (twin arginine transport)

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77
Q

type 2 secretion

A

gram neg, get past outer mem
use SecA and YEG to get protein to periplasm, then beta barrel pushes it out

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78
Q

type 5 secretion

A

gram neg, get past outer mem
similar to 2 but uses single peptide (instead of SecA and YEG) to push out, one peptide for all excretion functions

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79
Q

type 3 secretion

A

gram neg, get past outer mem
uses complex of many proteins in mem, span periplasm, form pore to outer mem, form needle to inject to host cell; No sec

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80
Q

bacterial growth phases

A

lag
exponential
stationary

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81
Q

how to calculate number of generations from growth numbers

A

3 gen = 10x inc
How many gen from 10 to 1000 bacteria > 10^2 inc > 3 gen = 10x, so 2*3 = 6 generations

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82
Q

biofilms

A

communities on solid/liquid environments
features: glycocalyx holds cells together, slowed metabolism,
resistant to antibiotics and host defenses, quorum sensing

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83
Q

glycocalyx

A

holds cells of a biofilm together

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84
Q

planktonic bacteria

A

free individual bacteria not part of biofilm

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85
Q

mesophile

A

bacteria that grow best at body temp (37’ C)

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86
Q

fastidious bacteria

A

require many nutrients provided to them

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87
Q

simple bacteria

A

make everything (nutrients) from scratch

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88
Q

features of bacterial genome

A

HAPLOID (no dom or recessive genes)
required: chromosome
optional: plasmids, bacteriophage, insertion seq, transposons

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89
Q

macro-mutation

A

affect >1 base (insertion, deletion, inversion, duplication)

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90
Q

effects of mutations

A

silent, loss of function, altered function
Completely new genes are not constructed by a single mutation, need many

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91
Q

importance of genetic exchange

A

antibiotic resistance, changes in virulence, changes in Ag makeup (avoid imm resp)

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92
Q

mechanisms of genetic exchange

A

transformation - uptake of naked DNA
transduction - bacteriophage as vectors
conjugation - plasmids moved by cell-cell contact

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93
Q

transformation

A

uptake of naked DNA
recipient must be competent to uptake DNA
DNA enters linear > digestion > recombine to be rescued and funct in recipient

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94
Q

natural v artifical competence

A

competence = ability to take up DNA
only certain bacteria are naturally transformable
electroporation is artificial

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95
Q

transduction

A

bacteriophage as vector

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96
Q

types of phage transduction

A

lytic - always lyses and kills host cell
temperate - can stably infect and coexist with host cell (lysogeny) until lytic phase is induced

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97
Q

lysogeny

A

exists in host - stably integrates and replicates in host

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98
Q

prophage

A

phage genome (lysogeny)

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99
Q

lysogen

A

bacterial cell that the phage is in (lysogeny)

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100
Q

lysogenic conversion

A

phage encodes an observable funct and induces it in infected host

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101
Q

specialized transduction

A

phage drags along piece of bacterial genome near integration site with it when it goes lytic and makes new phage
changes the next recipients genome when it integrates
specialized bc DNA near integration site

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102
Q

generalized transduction

A

phage accidentally packages random bacterial genome
when capsid injects, no phage, new genes recombine to cause change
caused by ‘sloppy’ capsid
generalized bc any random DNA (not specific to integration site)

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103
Q

lysogenic conversion v specialized transduction v generalized transduction

A

lysogenic conversion – gene started as part of phage and was integrated
specialized transduction – gene started as part of bacteria, transferred w phage DNA (near integration sites)
generalized transduction – transfer of bacterial genes via phage (random DNA), with no phage DNA

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104
Q

conjugation features

A

plasmids moved by cell-cell contact
sex pilus > cell to cell contact via pilus > COPYING plasmid DNA and transfer of copy into recipient cell
(BOTH donor and recipient have copy of plasmid)

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105
Q

plasmid features

A

non chromosomal DNA, usually circular, transmissible via conjugation, important for virulence and antibiotic resistance

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106
Q

types of conjugation

A

conjugative - plasmid encodes all functs for conjugation and can move itself
mobilizable - needs help to move
non-transmissible - can’t move by conjugation

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107
Q

conjugative plasmids

A

plasmid encodes all of the functions for conjugation and can move itself from the donor cell to the recipient cell

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108
Q

mobilizable plasmids

A

plasmid cannot move itself, but can be moved with help from a conjugative plasmid

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109
Q

non-transmissible plasmids

A

can’t move by conjugation

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110
Q

F+ (conjugation)

A

donor, male, contains conjugative plasmid
DO NOT CORRELATE WITH PRESENCE OR ABSENCE OF F PLASMID

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111
Q

F– (conjugation)

A

recipient, female, receives the plasmid
DO NOT CORRELATE WITH PRESENCE OR ABSENCE OF F PLASMID

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112
Q

Hfr

A

high freq of recombination
plasmid integrates into chromosome, conjugation will move part of the chromosome into the recipient

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113
Q

F’

A

excised plasmid w additional donor DNA accidentally brought with it (kinda similar to specialized transduction)
important for E coli

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114
Q

phage v plasmid DNA transfer

A

plasmids are more promiscuous in their host range

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115
Q

R plasmid

A

resistance genes
multiple resistances
rapidly transferred to diverse bacteria
transposons

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116
Q

transposition

A

move from one site in DNA to another within the same cell

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117
Q

Insertion seq (IS)

A

gene encoding transposition enzyme (transposase) flanked by inverted repeats of DNA sequence
can interrupt genes if they insert into them

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118
Q

transposon (Tn)

A

gene encoding observable funct flanked by two copies of an insertion seq
can move genes between chromosomes and plasmids or between diff plasmids
can result in plasmids with multiple antibiotic resistance

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119
Q

phase v antigenic variation

A

phase variation - change in seq leads to On-Off or A-B switch of two diff genes, caused by inversion of a DNA seq
Antigenic variation - change in DNA seq leading to switch of expression among multiple possible genes

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120
Q

phase variation

A

change in DNA seq leads to an ON-OFF or A-B switch of two diff genes
caused by inversion of a DNA seq

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121
Q

antigenic variation

A

change in DNA seq leading to switch of expression among MULTIPLE genes
most common -cassette model

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122
Q

Casette model

A

antigenic variation
non-expressed copies (silent) of a gene (the cassettes) are copied or recombined into a site where the cassettes can be expressed

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123
Q

operon

A

region of DNA (genes and required cis-active sites) expressed from same promoter therefore on same mRNA
(Bacteria can have polycistronic operons)

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124
Q

cistron

A

a single gene

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125
Q

regulon

A

regulated by same regulator

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126
Q

stimulon

A

regulated by same stimulus

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127
Q

catabolite repression thourgh CAP

A

global regulatory mech
CAP = activator
cAMP present in low ATP
cAMP binds CRP/CAP to activate it
CRP-cAMP binds DNA, can recruit RNA Pol
CRP regulon genes usually have weak promoters (low RNA pol binding), need 2 levels of regulation to activate

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128
Q

lacUV5

A

mut lac operon promoter
not sensitive to catabolite repression

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129
Q

trp-lac fusions

A

mut lac operon promoter
tac promoter stronger
trc even stronger
make it easier to express lac operon

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130
Q

Arabinose operon overview

A

pBAD promoter expresses araB, araA, araD
araC encodes activator AraC
CRP binding site: identical to lac operon
2 operators (pBAD and pC)
araI additional AraC binding site
AraC can be P1 (anti-activator) w/o arabinose or P2 (activator with arabinose)

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131
Q

arabinose operon - no arabinose

A

AraC in P1 form binds araO2 and araI > forms bend in DNA > prevents transcription
AraC P1 represses its own synthesis at araO2

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132
Q

arabinose operon - with arabinose

A

AraC in P2 form binds to araI > activating pBAD > activation
CRP + cAMP must ALSO bind to relieve catabolite repression

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133
Q

trp operon

A

TrpR repressor only binds to the operator and represses ptrp in the presence of Trp (corepressor) –> prevents syn of trp in presence of trp
has attenuation mediated by B:C (no trp) or C:D (trp) pairing
activation in 2 parts: trp binding trpR repressor and trp causing C:D pairing

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134
Q

trp operon - no trp

A

ribosome stalls b/c no trp in environment,
enables B:C pairing, no C:D

135
Q

trp operon - with trp

A

ribosome moves through all the way to stop codon
prevents B:C pairing
enables C:D –> acts as factor- independent terminator

136
Q

two component regulatory systems

A

affect transcription
Usually 2 proteins
Sensor (S, His kinase) and Receiver (R, transcriptional regulator, regulated by phosphorylation)
Both domains can be on same protein
often span cell mem
phosphorylation of S > transfer to R > R eff funct

137
Q

selective toxicity

A

toxic to bacteria but not humans, based on diff in physiology

138
Q

therapeutic index

A

toxic to human / therapeutic against bacteria
want large toxic dose and small therapeutic dose –> high index

139
Q

allergenicity vs toxicity

A

allergen dependent on indviduals imm sys
toxicity affects all of us

140
Q

MBC

A

minimum bactericidal conc
lowest dose for complete killing
want low dose
measured by serial dilution and plating
only for bactericidal antibiotics

141
Q

MIC

A

minimum inhibitory conc
lowest dose for statsis
measured by serial dilution and turbidity
want low dose

142
Q

bactericidal vs bacteriostatic

A

cidal –> kill (irreversible)
static –> stop growth (reversible)
static drugs will allow growth again after they are removed

143
Q

organ important for excretion of antibiotic

A

kidneys

144
Q

organ important for metabolism of antibiotic

A

liver

145
Q

broad vs narrow spectrum antibiotic

A

broad good for unknown bacterial agent with serious effects
narrow (specific) good for known bacterial agent

146
Q

where are the majority of antibiotics used

A

agriculture as growth supplement

147
Q

mechanisms of antibiotic resistance

A

enzymatically modify or degrade the antibiotic
alter the target of the antibiotic
pump out antibiotic
dec uptake
innate resistance

148
Q

bla gene

A

beta lactamase
can be counteracted w clavulanic acid

149
Q

cat gene

A

chloramphenicol acetyl transferase

150
Q

aph gene

A

aminoglycoside phosphotransferase

151
Q

what is the most common way to alter the target of an antibiotic to develop resistance

A

spontaneous mutations (retain original funct)

152
Q

example of enzymatic modification

A

methylation of rRNA, gives erythromycin resistance

153
Q

example of new biosynthetic pathway yielding altered target

A

vancomycin resistance,
cannot inhibit D-ala-D-lac (usually targets D-ala-D-ala) – not a point mut, too big a change

154
Q

example of acquiring new enzymes that are resistant

A

MRSA, permanent change in genome in the penicillin binding proteins (PBPs), likely from diff organism via horizontal gene transfer before antibiotics were being used

155
Q

example of pump out antibiotic

A

tetracycline resistance (tetA)
multiple antibiotic resistance (MAR, broad spectrum, pumps out many things)

156
Q

example of decreased uptake

A

smaller specific porins - multiple antibiotic resistance (MAR)

157
Q

example of innate resistance

A

Gram neg cannot take up large molecules
Wall-less don’t have peptidoglycan to target

158
Q

plasmid vs chromosomal resistance

A

plasmid: new enzyme to modify/pump,
new enzyme to modify target, new biosynthetic pathway/target
point mut: target changed, not recognized by antibiotic, retains cellular function

159
Q

common spontaneous point mutations

A

gyrA - DNA gyrase, resistant to nalidixic acid
rpsL - ribosomal protein, resistant to streptomycin
rpoB - RNA pol, reistant to rifampin

160
Q

why use multiple antibiotics for TB

A

high mut rate allows for antibiotic resistance

161
Q

infectious disease definition

A

cycle of biological interactions between pathogen and host
requires damage

162
Q

colonization definition

A

Presence of microorganisms without disease at that point, applies to surfaces only (skin, mucosal epithelium, but not blood)

163
Q

2 definitions of infection

A

in patients: disease (opposite of colonization)
in site of body: presence of microbes (disease or not)

164
Q

carrier state

A

colonization w pathogen

165
Q

overt pathogen

A

strict, primary
high probability of causing disease in an otherwise healthy host

166
Q

opportunistic pathogens

A

low probability and usually require a debilitated or compromised host (not necessarily immunocompromised)

167
Q

normal flora definition

A

frequently found on or within the body of healthy persons
can cause disease under right conditions
presence of bacteria doesn’t mean disease

168
Q

features of microbiota

A

microorganisms in or on body
not always healthy
can change
can affect many things:
metabolism/weight, immunity, resistance/susceptibility

169
Q

microbiota v microbiome

A

Microbiota are the organisms
Microbiome is the genomes of the microbiota

170
Q

common colonized sites

A

alimentary/intestinal tract
upper (not lower!) respiratory tract
distal genitourinary tract
skin

171
Q

common sterile sites

A

blood
CSF
interstitial fluid and spaces
lymph (not active infection/draining)

172
Q

how can normal flora cause disease

A

disruption of barriers
ex: endocarditis with oral streptococci
peritonitis after bowel trauma

173
Q

protective effects of normal flora

A

priming immune system
adaptive - Ab against nonpathogens that cross-react with pathogens
innate - integrity of gut and production of cytokines
exclusion of pathogens from colonized surfaces
release of SCFAs and bile acids
release of antimicrobial peptides

174
Q

non immune features of gut microbiota

A

degradation of dietary and mucosal polysaccharides (metabolism)
release of SCFAs
immune modulatory, metabolism
production of vitamins B and K
modification of bile acids

175
Q

7 stages of pathogenesis

A
  1. encounter
  2. entry
  3. spread (+/-)
  4. multiplication
  5. evasion of host defenses
  6. damage
  7. outcome:
    (7a) transmission to new host (+/-)
    (7b) recovery and treatment (+/-)
176
Q

exogenous v endogenous infections

A

Exogenous – disease started soon after encounter
Endogenous – stable relationship with normal flora broke down
some microbes can be endogenous or exogenous (person A has endogenous but spreads to person B, exogenous in person B)

177
Q

most common areas of entry

A
  1. mucosal mem (ingestion, inhalation, sex)
  2. skin surface
  3. direct inoculation (trauma, bite, injection, surgery)
178
Q

key features of adherence

A

mucosal surface moving fluid, must stick
specific ligand-receptor interactions - not generic
virulence factors
structures: pili/fimbriae, fibrillae
surface proteins
extracellular matrix polysaccharide and lipoteichoic acid of oral streptococci

179
Q

key features of spread

A

movement from surface through tissues / body
not all bacteria spread to cause disease
bacteria CANNOT penetrate intact skin
mucosal surface is usually first barrier
cellular v tissue invasion

180
Q

types of cellular invasion

A

enter professional phagocytes (MOs and neutrophils) by phagocytosis
enter non-phagocytes by bacterial mediated endocytosis resulting in phagosome/endosome (can involve type 3 secreted proteins - injected into host cell affecting actin polymerization)
other: escape phagosome to cytoplasm

181
Q

what is the role of type 3 secreted proteins in bacterial spread

A

non phagocytic cellular invasion
type 3 has needle structure, can allow injection of proteins that affect actin polymerization, can cause apoptosis

182
Q

key features of tissue invasion

A

between cells by:
– degrade extracellular matrix
– disrupt tight junctions
can use host cells to move through blood or lymph (intracellular pathogens)

183
Q

key features of multiplication

A

often needed for disease
environmental variance
inoculum size
incubation period (time between inoculation and disease)
ability to aquire Fe

184
Q

environmental variance of multiplication

A

tissue: intestinal lumen, blood, urine
intracellular bacteria:
cytoplasm (nutrient rich) vs. phagolysosome (nutrient poor)
presence of Fe

185
Q

how does Fe affect bacteria

A

acquisition of Fe from host transferrin, lactoferrin, or other Fe-binding proteins
bacteria use siderophores as virulence factors

186
Q

how does polysaccharide capsules evade complement

A

do not bind and/or activate complement

187
Q

how does M protein of streptococci evade complement

A

inhibition of activation and amplification cascade
M protein in fibrillar layer binds human H factor > downregulates complement

188
Q

how does smooth LPS evade complement

A

keep activation away from mem

189
Q

how does protease evade complement

A

degrade the complement

190
Q

what does C3b do in complement

A

opsonization

191
Q

what does C5-9 do in complement

A

lysis of gram neg (not pos)
membrane attack complex (MAC)

192
Q

what does C3a do in complement

A

inflammation

193
Q

what does C5a do in complement

A

inflammation

194
Q

extracellular antiphagocytic functs

A

inhibit recruitment via inhibition of complement and cytokines
kill the phagocytes via toxins
prevent phagocytosis by preventing opsonization, prevent binding (carbohydrate capsules)

195
Q

intracellular antiphagocytic functs

A

inhibit phagosome-lysosome fusion
escape phago(lyso)some into cytoplasm
inhibit oxidative burst
resist antimicrobial functions

196
Q

oxidative burst

A

rapid release of ROS, superoxide and hydrogen peroxide (H2O2)
NADPH oxidase makes superoxide, inhibiting it makes host susceptible to infections

197
Q

intracellular antimicrobial functs

A

oxidative burst
acid/pH
lysozyme
defensins (cationic proteins)

198
Q

what does lysozyme do

A

break down peptidoglycan backbone

199
Q

Ag mimicry vs Ag cloaking

A

Mimicry – surface looks like host
Cloaking – bind host and cover themselves with it

200
Q

Ag variation vs Ag variety

A

variation - change in real time, casette model (flu is exception where it is not real time)
variety - numerous already existing stable strains

201
Q

ways to avoid Ab detection

A

Ag mimicry, Ag cloaking, Ag variation, Ag variety, degradation of Abs

202
Q

modifications of cell mediated immunity

A

alter host response from cell-mediated (Th1) to antibody (Th2) response

203
Q

necrosis v apoptosis

A

necrosis - death by lysis; via toxins (outside) or intracellular growth (inside)
apoptosis - programmed death; type 3 secreted proteins

204
Q

what is the main way in which bacteria damage the host

A

non specific immunopathology: inflammation, abscess, cytokines

205
Q

types of bacterial damage

A

cytotoxicity via necrosis or apoptosis –> cell death
altered pharmacology/physiology –> damage w/o cell death, can still lead to disease (and even death) on host level

206
Q

example of specific immunopathology

A

cell mediated or Abs made in response to bacteria that damage the host

207
Q

Reiter’s syndrome

A

Heat shock protein from bacteria > imm resp > causes response to host HSPs

208
Q

cytokines that damage host from endotoxins

A

TNFalpha (vascular epithelium, vasodilation, permeability)
IL1 (fever)
IL6 (acute phase, liver)

209
Q

endo v exotoxins

A

endo = LPS (gram neg only)
exo = A-B proteins

210
Q

A-B proteins

A

A=active portion, B=binding portion

211
Q

exotoxin mechanisms

A

lysis (ex: pores), cytotoxicity (ex: altered protein syn), pharmacological (ex: cAMP levels)
extracellular enzymes (ex: protease, lipase, hyaluronidase)
superAgs
type 3 secreted proteins (apoptosis, actin polymerization)

212
Q

super Ags

A

stimulate host T cell resp in Ag-independent manner
binding to Vbeta of T cell receptor resulting in cytokine cascade - similar to endotoxin

213
Q

key features of bacterial transmission

A

transmission ‘completes cycle’
not required for disease/pathogenesis

214
Q

generic enteric bacteria - encounter

A

HUMAN FECAL contamination of food and water (direct, water, soil)
“NATURALLY” INFECTED ANIMAL FOODS - meats, dairy products, seafood (usually from processing not the animal itself)
ENVIRONMENTAL - Contamination of food with soil (usually fruits and vegetables)

215
Q

generic enteric bacteria - entry

A

oral

216
Q

generic enteric bacteria - spread

A

3 options: 1. no spread past intestinal epithelium, 2. invade lateral w/i intestines, 3. invade deeper to draining lymph, blood, etc

217
Q

generic enteric bacteria - multiplicaiton

A

lots of food, but little or no oxygen in LARGE INTESTINE
chemical barriers to growth and multiplication - acid, bile
competition from normal flora
intracellular pathogens have difficult hurdles

218
Q

generic enteric bacteria - evade imm defense

A

STOMACH - acidity; stomach is practically sterile
SMALL INTESTINE- low inoculum from stomach; digestion (especially bile), peristalsis (movement of intestine) prevents colonization
LARGE INTESTINE - normal flora made up of obligate anaerobes and some facultative anaerobes
IMM DENSES - phagocytes during inflammation; antibacterial peptides (cryptdins and defensins in crypt cells)
ADAPTIVE IMM - only sIgA (important for newborns)

219
Q

generic enteric bacteria - damage

A

toxins
invasion of epithelium
inflammation
attaching-effacing adherence
vomiting
diarrhea
dysentry

220
Q

vomiting features

A

rapid onset
usually toxin

221
Q

diarrhea features

A

large volume, usually w/o blood or pus
usually small intestinal effects (secretory bowel)
usually from toxin
bloody diarrhea does not equal dysentery

222
Q

dysentery features

A

hallmark = WBCs in stool
smaller volume, pus (WBCs), +/- blood, fever, abdominal pain
usually from large intestine (inflammatory bowel)
usually invasive organisms

223
Q

diseases associated w dysbiosis

A

inflammatory bowel disease, irritable bowel syndrome, Crohn’s disease

224
Q

hygiene theory

A

cleaner upbringing results in less microbiota interactions, inc incidence of allergies

225
Q

treatments to manipulate the microbiota

A

fecal transplant
probiotics (microbes in food)
prebiotics (compounds supporting microbes)
antibiotics
diet

226
Q

food intoxication

A

no infection needed
toxin is preformed in food from contamination

227
Q

Staphylococcus aureus features

A

gram pos, coccus
rapid onset, profuse vomiting, possible diarrhea
food intoxication caused by preformed toxin

228
Q

Staphylococcus aureus - encounter

A

infected food handler (human reservior) that shed toxin into food

229
Q

Staphylococcus aureus - damage

A

enterotoxins released into food act as heat stable SUPERANTIGENS

230
Q

Clostridium botulinum features

A

gram pos rod
obligate anerobe
spore formation
preformed spore causes botulism
can also cause infant and wound botulism (rare)

231
Q

Clostridium botulinum - encounter

A

spores from soil-contamination (i.e., vegetables) germinate in anaerobic but incompletely processed CANNED (autoclaved) food

232
Q

Clostridium botulinum - damage

A

botulinum toxin (neurotoxin) that inhibits Ach
symptoms follow pattern: ocular > pharyngeal > respiratory paralysis > death

233
Q

Botulinum toxin features

A

neurotoxin - causes flaccid paralysis by inhibiting release of acetylcholine (Ach is excitatory
A-B type; heat labile
encoded on LYSOGENIC BACTERIOPHAGE

234
Q

Clostridium botulinum - treatment

A

supportive therapy (respiratory), anti-toxin

235
Q

toxinogenic infections

A

not caused by preformed toxins but actual infections

236
Q

Vibrio cholerae features

A

gram neg comma shaped bacterium
classified by O Ag of LPS (O:1 is epidemic)
asymptomatic, mild , or severe
severe causes rice water stool, death by dehydration

237
Q

Vibrio cholerae - encounter

A

contaminated water, vegetables
environmental or human
not endemic to US

238
Q

Vibrio cholerae - entry

A

pili as adherence factors

239
Q

Vibrio cholerae - spread

A

none within body
localized to epithelial surface
(fecal - oral between hosts)

240
Q

Vibrio cholerae - damage

A

chloera toxin
causes constitutively active adenylate cyclase > inc cAMP > diarrhea from secretion of water and salts
no cellular damage, cells can still absorb (give fluids to treat)

241
Q

Chloera toxin features

A

A-B type toxin (1A and 5B)
B portion binds to GM1 gangliosides of host cells
A portion has ADP-ribosylates stimulatory G protein of adenylate cyclase –> constitutively active –> inc cAMP
causes secretion of water and salts into lumen of intestine
absorptive functions intact; no cellular damage
LYSOGENIC CONVERSION

242
Q

Vibrio cholerae - evade imm defense

A

no immunological denfenses in naive host
vaccine exists but not good –> killed V. chloera injected IM, makes IgG resp not IgA resp

243
Q

Vibrio cholerae - treatment

A

oral or i.v. fluid and electrolyte replacement and antibiotics
vaccine exists but not good –> killed V. chloera injected IM, makes IgG resp not IgA resp, working on live attenuated oral vacc

244
Q

EHEC features

A

gram neg
can cause bloody diarrhea and hemolytic-uremic syndrome
EHEC = O157:H7 serotype
O = O Ag of LPS
H = H Ag (flagella)

245
Q

EHEC - encounter

A

contaminated food from animals, mainly beef, also apple cider (and swimming pools)
bovine fecal contamination
endemic to US

246
Q

EHEC - entry

A

resistant to stomach acid (low infectious dose needed to cause disease)
adherence through specialized mechanism
attaching-effacing lesion –> formation of pedestal by polymerization of actin

247
Q

EHEC - damage

A

although bloody diarrhea appears like invasive dysentery (e.g., Shigella), the bacteria do not invade the epithelium, therefore little fever or pus in stool
secrete a Shiga-like toxin (SLT/Stx)
causes severe tissue damage in the large intestine, distal ileum because of capillary thrombosis (clots)
diarrhea caused by type 3 secreted proteins that stimulate ATP secretion and inc adenosine in lumen > fluid secretion

248
Q

Hemolytic uremic syndrome

A

caused by EHEC
mainly in very young
SLT in blood
damage to endothelial cells of the vasculature or kidneys
renal endothelial damage
microangiopathic hemolytic anemia
thrombocytopenia
thrombosis of glomerular capillaries

249
Q

EHEC - treatment

A

Symptomatic and supportive
Avoid antibiotics because they can stimulate SLT/Stx from phage and cause HUS

250
Q

Clostridium difficile features

A

gram pos, obligate anaerobe, spore former
causes Antimicrobial Associated Diarrhea aka Pseudomembranous Colitis
associated w antibiotic treatment and hospital stays

251
Q

Clostridium difficile - encounter

A

dysbiosis of normal flora from antibiotics
nosocomial infections

252
Q

Clostridium difficile - damage

A

toxins A and B (NOT A-B txn)
Toxin A - inc mem permeability and inflamm in intestinal mucosa
Toxin B - cytotoxin, necrosis and epithelial destruction
mild/watery to bloody diarrhea to inflammation and ulceration
recent emergence of highly virulent strains

253
Q

Clostridium difficile toxins A and B

A

toxins A and B (NOT A-B txn)
Toxin A - inc mem permeability and inflamm in intestinal mucosa
Toxin B - cytotoxin, necrosis and epithelial destruction

254
Q

Clostridium difficile - treatment

A

antibiotics
fecal transplant (recurrent infections)

255
Q

Shigella dysenteriae and flexnerii features

A

gram neg rods, enteric
diarrhea, progresses to dysentery (blood and pus), abdominal pain, tenesmus (cannot defecate), fever

256
Q

Shigella dysenteriae and flexnerii - encounter

A

humans only dysenteriae NOT endemic to US
flexneri is endemic

257
Q

Shigella dysenteriae and flexnerii - entry

A

highly acid resistnatsmall unoculum
infection in colon

258
Q

Shigella dysenteriae and flexnerii - spread

A

laterally in intestines
(fecal-oral from host to host)

259
Q

Shigella dysenteriae and flexnerii - damage

A

PLASMID-encoded cellular invasion of epithelial cells of the colon (type 3 secretion)
lyse vacuole and replicate in cytoplasm
– use host actin polymerization to move directly
from cell to cell by puncturing host
cause cell death (cytotoxicity) and ulceration, inflammation

260
Q

Shiga toxin

A

Stx
ONLY dysenteriae
A-B toxin
A = inactivates ribosomes (deglycosylates rRNA) halting protein syn and killing the host cell
associated with hemolytic uremic syndrome
similar to EHEC
do NOT treat with antibiotics
dysenteriae is NOT endemic to US

261
Q

Shigella dysenteriae and flexnerii - evade imm defense

A

intracellular location –> sequestered from phagocytes
if MO around, can cause apoptosis
no vaccine

262
Q

salmonella enterica typhi and paratyphi features

A

gram neg
thousands of serotypes
typhoid (enteric) fever is most severe
gastroenteritis is most common
septicemia, focal infections
carrier state
few intestinal symptoms, mainly systemic (fever, shock, headache, myalgia, lethargy, splenomegaly, hepatomegaly)

263
Q

salmonella enterica typhi and paratyphi - encounter

A

only in humans
indirect spread (water, food)
S. Typhi not endemic to US, S. Paratyphi is

264
Q

salmonella enterica typhi and paratyphi - spread

A

invades GALT of small intestine
transcytosis through epithelial cells
infects lymph nodes, blood, spleen, liver, bone marrow, other focal organs (e.g., gall bladder)

265
Q

salmonella enterica typhi and paratyphi - evade imm defense

A

resistant to phagocytes (intracellular)
resistant to complement
cell-mediated immunity more important
S. typhi (not paratyphi) have Vi capsular Ag (odd for intracellular bacteria)
killed IM vacc not good (bc induce IgG)
working on live attenuated oral vacc

266
Q

salmonella enterica typhi and paratyphi - damage

A

endotoxin (LPS) and inflammation

267
Q

non-typhoid salmonellosis features

A

predominantly S. typhimurium and S. enteritidis
nausea progressing to diarrhea and severe abdominal pain, can be dysentery in severe cases, infrequent bacteremia in healthy, but recurrent bacteremia in immunocompromised (AIDS)
can become systemic

268
Q

non-typhoid salmonellosis - encounter

A

not human specific (human to human possible)
found in animals (poultry and bovine)

269
Q

non-typhoid salmonellosis - spread

A

invade the epithelial cells of the small intestine using adherence factors and invasion factors to stimulate endocytosis by host (type 3 secretion)
transcytosis through epithelial cells
infection usually limited to intestines

270
Q

non-typhoid salmonellosis - multiplicaiton

A

virulence plasmid inc growht rate in MO

271
Q

non-typhoid salmonellosis - evade imm defense

A

resistant to phagocytes (intracellular)
resistant to complement (LPS)

272
Q

non-typhoid salmonellosis - damage

A

inflammatory diarrhea (not toxin)
type 3 secretion
inflamm and endotoxin for systemic infections

273
Q

non-typhoid salmonellosis metastatic infection

A

fever, shock, endotoxin
localized metastatic disease
gastroenteritis symptoms

274
Q

non-typhoid salmonellosis asymptomatic carrier state

A

asymptomatic
can last as long as 20 weeks

275
Q

effects of STIs

A

infertility
chronic pelvic pain
cervical cancer
liver disease
perinatal morbidity
childhood blindness
ectopic pregnancy

276
Q

STI prevalence

A
  1. chlamydia
  2. gonorrhea
  3. syphilis
    chlamydia is most common
    syphilis is most severe w long lasting side effects
277
Q

core individuals (STIs)

A

one person who spread to many people (promiscuous individuals)

278
Q

STI featues

A

encounter - human only, labile to environment
theoretically eradicable
entry - mucous mem mostly, some blood
intracellular
no vacc

279
Q

Neisseria gonorrhea culture

A

normal media

280
Q

chlamydia trachomatis culture

A

tissue only, obligate intracellular

281
Q

treponema pallidum culture

A

not culturable

282
Q

chlamydia trachomatis features

A

gram neg, obligate intracellar
many serovars
one of most common bacterial infections in US
urethritis, cervicitis, endometritis, salpingitis, epididymitis, prostatisis
pelvic inflammatory disease (infertility, ectopic pregnancy, chronic pelvic pain)
lymphogranuloma venereum (certain serovars – not endemic to US)

283
Q

Chlamydia trachomatis - encounter

A

human only
sex, birth

284
Q

Chlamydia trachomatis - entry

A

genital, anal, columnar epithelium

285
Q

Chlamydia trachomatis - spread

A

invasion of epithelium
exit via endolysosomal pathway
MTs > peri-golgi > MT organizing center

286
Q

Chlamydia trachomatis - multiplication

A

obligate intraceullar
elementary (entry) > inclusion > reticulate > elementary > exit
elementary = infective, non replicative
reticulate = non infective, replicative, alter endosomal mem fro transport

287
Q

Chlamydia trachomatis - damage

A

inflammation
often asymptomatic (females don’t always notice infection bc internal)

288
Q

Chlamydia trachomatis - diagnosis

A

PCR
can’t culture

289
Q

Chlamydia trachomatis - treatment

A

antibiotics

290
Q

neisseria gonorrhoeae features

A

gram neg diplococcus
urethritis, cervicitis, endometritis, salpingitis, epididymitis, prostatitis, proctitis, pharyngitis
pelvic inflammatory disease, infertility, ectopic pregnancy, chronic pelvic pain
Disseminated Gonococcal Infection (DGI)
– dermatitis, arthritis, tenosynovitis

291
Q

Disseminated Gonococcal Infection (DGI)

A

spread to other parts of body
can cause dermatitis, arthritis, tenosynovitis

292
Q

neisseria gonorrhoeae - encounter

A

human only
sex, birth

293
Q

neisseria gonorrhoeae - entry

A

genital tract, oral, anal, ocular
columnar epithelium
pilus
Opacity proteins (Opa)

294
Q

neisseria gonorrhoeae - spread

A

does not have to
some strains invade – Disseminated Gonococcal Infection (DGI)
invasion of epithelial cells via transcytosis

295
Q

neisseria gonorrhoeae - multiplication

A

fastidious
chocolate agar, thayer-martin (selective)
needs elevated CO2

296
Q

neisseria gonorrhoeae - evade imm defense

A

antigenic variation: pilus via cassette model and opacity proteins (Opa) via slip-stranded (post-transcriptional)
IgAse
serum resistance (DGI) via LPS + sialic acid

297
Q

how does pili affect gonorrhoeae

A

Ag variation
casette model

298
Q

how does Opa affect gnorrhoeae

A

Ag variation
slip-stranded mutagenesis –> 5’ has CTCTT repeat, slipping can add or delete repeats > frameshift
Post translational

299
Q

neisseria gonorrhoeae - damage

A

inflamm
purulent exudate (pus)
often asymptomatic (esp female)

300
Q

neisseria gonorrhoeae - diagnosis

A

PCR or culture
PCR is more common, culture used to test antibiotic sensitivity

301
Q

neisseria gonorrhoeae - treatment

A

antibiotics

302
Q

treponema pallidum features

A

gram neg spirochete
cause syphilis
very labile
need darkfield microscopy / fluorescence
has 1’ (local), 2’ (disseminated), and 3’ (latent) stages
if congenital –> lethal or defects

303
Q

syphilis stages

A

1’ = local chancre, 3 wks
2’ = 1/2, disseminated mucocutaneous skin lesions, 3 mo
can go latent, yrs, 2/3
3’ = ½ of latent; bone, blood vessels, brain, gummas (granulomas)

304
Q

treponema pallidum - encounter

A

human
sex, congenital, birth

305
Q

treponema pallidum - entry

A

GI mucous mem
epidermal abrasions
inf endothelim

306
Q

treponema pallidum - spread

A

motility via periplasmic flagella
flagella are internal

307
Q

treponema pallidum - damage

A

vasculitis
3’ causes imm rxns

308
Q

treponema pallidum - diagnosis

A

serology – screen (anti-cardiolipin) then specific (treponemal)(cannot culture)

309
Q

treponema pallidum - treatment

A

antibiotics
do not help 3’ stage infection

310
Q

stages of sepsis

A

SIRS (Systemic Inflammatory
Response Syndrome) > Sepsis (SIRS + infection) > Severe Sepsis (sepsis + organ dysfunct or low BP) > Septic Shock (sepsis + hypotension despite resuscitation)

311
Q

multiorgan system dysfunct

A

organ failure
Overlaps w septic shock
Clotting disorders or failure of renal, hepatic, cardiac, or cognitive funct
Accumulation metabolism byproducts that cannot be cleared (e.g., lactic acidosis)

312
Q

why inc in sepsis

A

people living more (aging, immunocompromised, etc)
more invasive procedures and surgeries
antibiotic resistance
inc diagnosis
results in more gram pos (normal flora) and more fungi than before

313
Q

causes of sepsis

A

Bacteria (and fungi) in blood
Not all bacteremia leads to sepsis
Certain virulence factors
Invasion through skin, mucosa
inc risk in those with Granulocytopenia, PMN dysfunction, Complement defects, Adaptive immunity defects (Ig and cell mediated), Splenic dysfunction

314
Q

sites of infection in severe sepsis

A
  1. lungs (from pneumonia)
  2. abdomen (from gut leaks)
  3. urinary tract
  4. soft tissues
  5. IV catheters
315
Q

host mediators of sepsis

A

inflamm cytokines
TNFalpha, IL1, IL6, IL8
causes fever, dec BP, inc capillary permeability flow, infiltration of neutrophils and
platelets, activation of the coagulation cascade
normal responses, just happening too much

316
Q

sepsis symptoms

A

abnormal temp, low BP, mental change, renal dysfunct, techypnea (respiratory), edema, dec capillary refill, vascular occlusion

317
Q

SIRS definition

A

Systemic Inflammatory Response Syndrome
Not necessarily due to infection

318
Q

Sepsis definiton

A

SIRS + proven or suspected infection

319
Q

Severe sepsis definition

A

sepsis + organ dysfunct (other than at site of infection), or hypoperfusion, or hypotension

320
Q

Septic shock definition

A

Sepsis with hypotension that persists despite adequate fluid resuscitation and therefore requires pharmacologic blood pressure
support (“pressors” like norepinephrine)
often w lactic acidosis

321
Q

PAMPs in sepsis

A

LPS, peptidoglycan, and flagella
recog by TLRs and NOD proteins

322
Q

NFkappaB

A

master regulator of inflammation
PAMPs trigger NFkappaB expression, cause cytokines, chemokines, adhesion, etc

323
Q

sepsis - damage

A

acting on vascular endothelim mostly
hypotension and capillary leak, dec perfusion, dec oxygen, accumulation of metabolites (lactic acidosis), organ dysfunct
neutrophil survival inc
Disseminated intravascular coagulation (DIC)

324
Q

sepsis - treatment

A

within 1 hour
fluid resuscitation
dopamine/norepinephrine for low BP
broad antibiotics
culture blood, urine, etc
remove foreign objects (catheters)

325
Q

ETEC disease

A

gram neg
Travelers diarrhea/watery diarrhea

326
Q

ETEC - encounter

A

fecal-oral
human

327
Q

ETEC - entry

A

oral, small intestines

328
Q

ETEC - evade imm defense

A

pili/fimbriae adherence factors
there are no innate defenses in the non-immune intestinal tract that ETEC must contend with

329
Q

ETEC - spread

A

no spread

330
Q

ETEC - multiplication

A

there are no special/unusual growth requirements during infection or in the lab

331
Q

ETEC - damage

A

Heat stable toxin, ST and heat labile toxin LT, fluid secretion
plasmid encoded

332
Q

ETEC - mechanism of action of the primary virulence factors

A

fluid secretion by increased cAMP/cGMP
plasmid encoded

333
Q

ETEC - outcome

A

recovery, usually even without treatment

334
Q

ETEC - treatment

A

fluid replacement
no current vacc, if making vaccine use live attenuated vaccine making pili and inactive toxins

GMS6121 - Infectious Diseases (4 decks)

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