Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BOD MVST 1b > Bacteriology > Flashcards

Bacteriology Flashcards

1
Q

What are Koch’s postulates?

A

A specific bacterium causes a specific disease so

  1. Bacterium must be present in every case of the disease
  2. Must be able to isolate the bacterium from the disease and grow it in pure culture
  3. Specific disease must be reproduced from pure culture in healthy susceptible host
  4. Bacterium must again be recovered
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How big are bacteria and how big are mammalian cells?

A

About 0.5-3 x 0.5 micrometers
Anthrax is big, 8-10 micrometers
Human 10-100micrometers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are nosocomial infections?

A

Hospital-borne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Who was Mary Mallon?

A

A carrier of typhoid

small percentage of salmonella typhi remained in her gallbladder, periodically shed in faeces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is an endemic disease

A

A disease that occurs regularly at low or moderate frequency

e.g. dental caries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is epidemic disease?

A

A sudden appearance of disease, or increase above the endemic level
e.g. diphtheria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is pandemic disease?

A

Global epidemic

e.g. cholera

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the modes of transmission?

A

Direct:

  • Horizontal (sexual, respiratory tract via droplets, contamination from own flora, contact with skin and eyes)
  • Vertical (transplacental, parturition)

Indirect:
- Inanimate objects (nosocomial, food intoxication or infection, water faecal-oral or air-con respiratory, animals, soil via spores)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Legionnaire’s

A

Legionella pneumophilia
Pneumonic disease
Contracted indirectly via water droplets in air con units

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name an obligate intracellular parasite bacterial infection

A

Chlamydia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How many genes do bacteria and mammals cause?

A

4500 genes, humans 22K gnees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the cytoskeleton like in bacteria and mammals?

A 
Bacteria = rudimentary, ancient homologue of actin
Mammals = extensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do bacteria move?

A

Rotating flagella

Extending/retracting pili

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do bacteria divide?

A

Binary fission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are bacterial genomes like? What are mammalian?

A

Haploid usually single and circular + plasmids, bacteriophage
Mammalian: diploid, haploid gametes. Multiple (linear) + mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are bacterial and mammalian mRNAs like?

A

Bacterial: polycistronic (co-linear), unstable
Mammalian: spliced introns out, 3’ polyA, 5’ cap, often stable, single genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you regulate transcription in bacteria and mammalian cells?

A

Bacteria transcription initiation

Mammals often post-transcriptional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do bacteria divide?

A

Binary fission:
Rods = divide on terminal axis –> get chains
Cocci = divide in all planes –> cluster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What shape are salmonella?

A

Rods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What shape are E coli?

A

Rods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What shape is vibrio cholera?

A

Curved rods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What shape is trepanoma?

A

Syphilis

Spiral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What shape is helicobacter?

A

Gastric ulcer

Spiral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which bacteria produce endospores?

A

Clostridium tetani
Clostridium perfringens
Clostridium botulinum
Bacillus anthraxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do you gram stain bacteria?

A

Crystal violet and iodine
Ethanol wash
Counterstain with safranin (pink)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the difference between gram positive and gram negative?

A 
\+ = thicker peptidoglycan wall
- = extra membrane so LPS, porins in it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which bacteria don’t gram stain and why? What do you use instead?

A

Mycobacteria = waxy lipid coat so called acid fast
Ziehl-Neelsen stain
Chlamydia and mycoplasma = non-gonococcal urethritis = no cell wall, difficult to culture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the structure of bacterial cell walls?

A

Peptidoglycan]NAG and NAM cross linked by short oligopeptides (pentapeptides), and also cross links vertically to link the sheets into a thick layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the periplasm?

A

Space between two membranes of gram -ve bacteria

Contains hydrolytic enzymes and components of transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is in the outer membrane of gram - bacteria?

A

Porins
Channels essential to import and export
LPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the components of LPS?

A

O antigen. Highly variable, generates different antigens and therefore serotypes. Important defence against host attack against complement and macrophages.
Core polysaccharide.
A antigen. Endotoxin. Released from dying bacteria. Triggers wide ranging immune response. Recognised by TLR4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the function of the capsule?

A

Prevents drying during droplet infection

Protects from complement and macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the clinical effect of lipid A?

A

Have to judge when to give antibiotics for patients with bacteraemia- otherwise massive endotoxin release could lead to shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How do proteins cross the inner cell membrane in bacteria?

A

N-terminal secretion signal and Sec pathway

Then additional export pathways across periplasm and outer membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is TolC?

A

An exit duct for large toxin proteins and noxious molecules like antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How often do E. Coli numbers double in lab culture?

A

20-30mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What concentration of bacteria can you just about see in a practical?

A

10^5/ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How do bacteria physically divide after chromosome duplication?

A

FtsZ, a tubulin ancestor involved in cell division localises at midcell, forms ring that tightens, then new membrane and peptidoglycan form at division site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Name 2 facultative anaerobes

A 
Staphylococcus (aureus, epidermidis)
Streptococcus (pyogenes, pneumonia, viridans)
E coli
Enterococcus faecalis
Salmonella
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Name 2 strict anaerobes

A

Clostridium

Bacteriodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Discuss the structure of the mechanism that rotates the flagellum

A

Universal joint motor that rotates 360 degrees
H+ switch (H+ into cell)
Rings around motor that stop the rotation from damaging the cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How do bacteria choose where to go?

A

Chemotaxis
Chemoreceptors at nose of cell –> histidine-aspartate phosphorelay –> flagellar motor switch –> CCW to swim, CW to ‘tumble’ and randomly change direction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How fast can bacteria move?

A

30 microns/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Define operon

A

Contiguous genes whose transcription is coupled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is HAP?

A

Histidine-aspartate phosphorelay signalling pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is global regulation?

A

Co-regulation of expression of regulons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Define regulon

A

A set of operons switched on and off by the same phosphorelays

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is quorum sensing?

A

Where some pathogens switch on their virulence genes when its population reaches a specific density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How does quorum sensing work?

A

Bacteria release small signal molecules and sense its concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What does pseudomonas aeruginosa switch on with quorum sensing?

A

Genes for swarming, polysaccharide production, biofilm formation, virulence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are K antigens of Salmonella and E Coli?

A

Capsular polysaccharide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How does the bacterial genome change?

A
  1. Mutations
  2. DNA rearrangements due to random capture and insertion of insertion sequences (through their own recombination system)
  3. Transposons (often have IS at their ends)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What can transposons encode that is useful to the pathogen? And necessary for itself?

A

Antibiotic/heavy metal resistance, virulence genes
DNA transfer genes
Plasmid replication genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are pathogenicity islands?

A

Genes required for infection and survival in the host are found in groups within the genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the evidence for pathogenicity islands having joined recently?

A

Differing GC content of surrounding chromosomal DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What does salmonella encode on its pathogenicity islands?

A

SP1 - entry to non-phagocytic cells

SP2 - survival in macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How do bacteria acquire and transfer DNA?

A
  1. Transduction - bacteriophage viruses transfer DNA
  2. Transformation - uptake DNA released from dead lysed bacteria
  3. Conjugation - direct transfer between two bacteria via a sex pilus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How was transformation discovered?

A

Released that dead capsulated Strep Pneumoniae transformed live non-capsulated bacteria into capsulated agents that could kill mice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Where is lactobacillus found?

A

Oral cavity, urethra/vagina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

TLR2

A

Recognises peptidoglycan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

TLR4

A

Recognises LPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

TLR5

A

Recognises flagellin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

TLR9

A

Recognises unmethylated DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Discuss virulence genes

A
  • Specialised: not constitutively expressed but switched on in response to host environmental signals, global regulation
  • carried on plasmids, bacteriophage and/or pathogenicity islands
  • encode proteins or other molecules that are exported and secreted or are delivered into host cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How do uropathogenic E Coli colonise the host?

A

P-pilus adhesin binds a kidney glycolipid receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the most common cause of UTIs?

A

E coli from the host’s own colon flora ascending

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How does UPEC cause disease?

A

Haemolysin forms pores

LPS triggers inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How does proteus cause infection?

A

Urease cleaves urea to ammonia, increases pH, salt precipitates out, causes kidney stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How are type 1 and P-pili assembled on UPEC?

A
  1. Pilus subunits pumped across inner membrane by SEC
  2. Chaperones transfer across to usher proteins with an adhesin at the top
  3. Another system pushes the pili out through the usher proteins far enough to interact with the kidney cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Why does UPEC recur?

A

superficial epithelial cells undergo exfoliation due to urine flow, UPEC can invade underlying immature cells where they persist as quiescent reservoirs and aren’t reached by antibiotics. Can then resurge and enter bladder lumen –> further acute infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

How does EPEC colonise the colon?

A
  • Interaction with host cytoskeleton
  • Injects effector cells using specialised needles – including Tir (translocated intimin receptor)
  • Bacterial surface protein intimin binds Tir
  • Subverts host cell signal transduction
  • Induces actin polymers to form a pedestal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Name some bacteria that form biofilms

A

Streptococcus mutans - caries
Staphylococci that colonise catheters
Pseudomonas aeruginosa tat colonise contact lenses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What can pseudomonas aeruginosa cause?

A

Burns
Wounds
Eye infections
Nosocomial UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Pseudomonas biofilms: where and what do they release?

A

Cystic fibrosis sufferers lungs

Alginate polysaccharide - protect biofilm from host immune response and antimicrobials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How does listeria colonise the host?

A

ZIPPER: bind, invasins mimic eukaryotic ligands like fibronectin (in host ECM that binds integrins), cytoskeletal rearrangement, receptor mediated endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What type of bacterium is listeria?

A

Gram +ve rod
Can cross BBB and can endanger fetus
Food borne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How does salmonella colonise the host? Where are the genes for this found?

A

TRIGGER: bacterial needles, bacterial effector proteins SipA SipC, some bind to actin, some subvert signalling pathways SptP, cytoskeletal rearrangement, internalisation
Genes found on SPI-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

How do listeria escape their entry vacuole?

A

Listeriolysin phospholipase

79
Q

How do listeria move?

A

COMET TAIL!!!!

ActA at one pole polymerises and so pushes the bacterium forwards

80
Q

What causes infectious blindness?

A

Chlamydia trachomatis

81
Q

What can chlamydia trachomatosis cause urogenitally?

A

Non-gonococcal urethritis
Acute prostatitis (inflammation caused by LPS)
Chronic pelvic inflammatory disease and infertility

82
Q

How big is the chlamydia genome?

A

900 genes
1.04Mbp
`

83
Q

How big is the salmonella genome?

A

4450 genes

4.85Mbp

84
Q

What is an EB?

A

Infectious elementary body of chlamydia

Low metabolic activity and cant replicate

85
Q

What is an RB?

A

Reticulate body

Replicates inside host cells

86
Q

What is the chlamydia replication cycle?

A
  1. EB attaches to host epithelial cell
  2. Injects Tarp with virulence needle
  3. Rearranges host cell cytoskeleton so endosome uptake
  4. EB differentiates into RB
  5. RB replicates
  6. RB-containing vacuole segregates from normal endosome pathway to become an inclusion
  7. RB produce EB and Rb
  8. Host cell lyses, release EB, infect more cells
87
Q

What is tarp?

A

translocated actin recruiting phosphoprotein

Triggers uptake of EB of chlamydia

88
Q

What is an inclusion?

A

A protective, nutrient rich vacuole that RB replicates in in the chlamydia life cycle

89
Q

Discuss staphylococcal and streptococcal enzymes

A 
Collagenase 
Hyaluronidase
Staphylokinase
Coagulase
DNAse
90
Q

What does streptococcus pyogenes form?

A

Pharyngitis
Other acute suppurative infections (tonsillitis, scarlet fever, puerperal fever, necrotzing fasciitis, erysipelas, impetigo, mastitis in cattle)

91
Q

How do bacteria counteract lactoferrin and transferrin iron sequestration?

A

Bind iron at a higher affinity than the host using iron-binding siderophores and reimporting them loaded into cells. Example pyoverdine secreted by pseudomonas aeruginosa

92
Q

How do bacteria counteract low pH caused by gastric acid, or bile salts?

A

Shingella and helicobacter pump H+ out of their cell, and/or produce NH3 by urease action
Eject bile salts from membrane by MDR pumps

93
Q

What is YopT and YopP?

A

Yersinia injects YopT protease, which targets small GTPases to disrupt the cytoskeleton, and YopP acetyltransferase that inhibits signalling, triggering apoptosis

94
Q

Which bacteria release cytolysins to kill mphages and what are the enzymes called?

A 
B pertussis
E coli - haemolysin
Pneumococcus - pneumolysin
Strep pyogenes - streptolysins O and S
Helicobacter pylori - VacA
95
Q

Where does legionella pneumophilia live?

A

Obligate intracellular parasite of amoebae

Within air conditioning water and macrophages

96
Q

How do bacteria counteract macrophages?

A
  1. Prevent uptake: paralyse macrophage by subverting function, inhibit chemotaxis by cleaving C5a, shield with antiphagocytic capsules, kill with secreted cytolysisn
  2. Survive inside mphage: interfere with phagosome maturation, resist oxidative burst
97
Q

How does salmonella use phase variation to evade the host immune system?

A

Swaps gene for flagellin
First state has a promoter that allows transcription of flagellin 1 and a repressor for flagellin 2.
Promoter flanked by recombination sequences, so gets inverted
Second state doesn’t allow transcription, so no repressor, and flagellin 2 synthesised

98
Q

What is the organism morphology of Neisseria gonorrhoea?

A

Gram - diplococci

99
Q

How does salmonella evade the host immune system?

A
  1. Interfere with phagosome maturation in macrophages
  2. Resist oxidative burst as waxy cell wall deflects lysosomal enzymes
  3. Phase variation of flagellin
100
Q

What does ‘toxoided’ mean?

A

Denaturing and so inactivating exotoxins

101
Q

What are the two groups of exotoxins?

A
  1. Cytolysins

2. Enzymatic intracellular toxins

102
Q

What does C. perfringens alpha toxin do?

A

secreted for enzymatic degradation of membrane phospholipids

103
Q

What are AB toxins? Why are they called that?

A

Enzymatic intracellular toxins
Poison host cells by specific catalytic activity
B subunit = receptor-binding
A subunit = intracellularly active components

104
Q 
Which AB toxins are single polypeptides, which are multimeric?
Anthrax
Tetanus
Botulinum
Cholera
Pertussis
Diphtheria
A

Single: diphtheria, tetanus, botulinum
Multimeric: anthrax, pertussis, cholera

105
Q

Discuss bordetella pertussis AB toxins

A
  1. ADP-ribosylate regulators of AC, disturb cAMP, signalling and ion balance
  2. Produce ACs that mimic mammalian enzymes
106
Q

How can AB toxins act?

A
  1. ADP-ribosylating
  2. Mimic mammalian AC
  3. Glycosidases that depurinate 28s rRNA, blocks protein synthesis
  4. Glucosylate small GTPases involved in signal transduction, disrupt actin cytoskeleton and tight junctions
  5. Cleave DNA with cytolethal distending toxins
  6. Deaminate host cell GTPases so disrupts signal transduction to reorganise actin cytoskeleton
107
Q

How does cholera toxin work?

A

ADP-ribosylates regulators of AC, disturb cAMP signalling and ion balance

108
Q

How does shinga toxin work?

A

Glycosidase that depurinates 28S rRNA so blocks protein synthesis

109
Q

How does diphtheria toxin work?

A

Targets translation elongator factor 2 by ADP-ribosylating it, so blocks protein synthesis

110
Q

How do E coli toxins work?

A

LT Labile toxin ETEC: ADP-ribosylates regulators of AC, disturb cAMP signalling and ion balance
Another one: Cytolethal distending toxin cleaves DNA
Another one: for E coli that causes meningitis. Deaminates host cell GTPases, disrupts signal transduction to reorganise the actin cytoskeleton

111
Q

How does bacillus anthraxis toxin work?

A

Produces AC that mimics mammalian enzymes

Disturb cAMP, signalling and ion balance

112
Q

How does pertussis toxin work?

A

ADP-ribosylates regulators of AC, disturb cAMP signalling and ion balance

113
Q

How does salmonella typhi toxin work?

A

Cytolethal distending toxin CDT, cleaves DNA

114
Q

How does C diff toxin work?

A

Glucosylates Rho/Ras GTPases involved in signal transduction. Disrupts actin cytoskeleton and tight junctions.

115
Q

How does UPEC toxin work?

A

Cytotoxic necrotising factor
Deaminase of host cell GTPases
Disrupts signal transduction to reorganise the actin cytoskeleton

116
Q

How does campylobacter toxin work?

A

Cytolethal distending toxin, cleaves DNA

117
Q

How does tetanus toxin work?

A

TeNT B chain binds to receptor on peripheral nerve membranes
A chain internalised and undergoes retrograde transport to CNS inhibitory interneurons
A chain cleaves synaptobrevin
Blocks release of inhibitory neurotransmitters
Uncontrollable muscle contraction, spastic paralysis

118
Q

How does botulinum toxin work?

A

BoNT binds to receptor on peripheral nerve terminals
Receptor mediated endocytosis
Proteolytic action on synaptobrevin on peripheral nerves
Prevents release of stimulatory neurotransmitters
Flaccid paralysis

119
Q

Discuss the pathogenesis of toxic shock syndrome

A

TSST S aureus in highly absorbent tampons

Superantigen

120
Q

What type of pathogen is Neisseria meningitides?

A

gram -ve coccus

121
Q

What type of pathogen is haemophilus influenza type B (hib)?

A

Gram -ve rod

122
Q

What type of granuloma forms for mycobacterium?

A

Th2 CD4

123
Q

What causes leprosy?

A

Mycobacterium leprae

124
Q

What causes syphilis?

A

Treponema pallidum (sperochaete)

125
Q

What causes Lyme’s disease?

A

Borrelia burgdorferi

126
Q

What causes diphtheria? What kind of bacterium is it?

A

Corynebacterium diphtheria

Gram + rod

127
Q

What kind of vaccination is used for diphtheria?

A

Toxoid vacccination

128
Q

What controls the diphtheria toxin?

A

Controlled by a bacterial TF DtxR, represses gene expression when bound by iron, so in the host (where iron is sequestered), turned on

129
Q

Where does corynebacterium diptheriae colonise?

A

Nasopharyngeal epithelium

130
Q

Which disease is associated with a respiratory pseudomembrane?

A

Diphtheria

131
Q

What is the mechanism of action of diphtheria?

A
  1. AB polypeptide binds to HB-EGF via B
  2. AB polypeptide nicked by host protease furin, but two remain covalently bound
  3. Toxin taken up by endocytosis
  4. V-ATPase proton pump acidifies endosome
  5. Triggers B-dependent translocation of A across vesicle membrane into cytosol
  6. Disulfide bond reduced in cytosol
  7. A released
  8. Blocks protein synthesis by ADP-ribosylating transcription elongation factor-2
132
Q

What causes pharyngitis?

A

Streptococcus pyogenes

133
Q

What are the virulence factors of streptococcus pyogenes?

A
  1. Colonisation
    Adhesins
  2. Damage causing
    a. polysaccharide capsule
    b. Surface M protein binds complement factor H
    c. C5a peptidase - inhibit mphage chemotaxis
    d. Streptolysisn O and S - pore-forming toxins
    e. Pyogenic toxins - superantigens
    f. Hyaluronidase - breaks down tissue (spread)
    g. streptokinase - lyses clots (spread)
    h. DNAse - depolymerises DNA in puss (reduces abscess viscosity)
134
Q

What complications can acute pharyngitis lead to?

A

Rheumatic fever. Believed to involve autoimmunity e.g. to M protein. Heart and joint granulomas, plus fever
Glomerulonephritis. Type III hypersensitivity. Accumulation of Ab-Ag complexes that lodge in kidney glomeruli –> inflammation

135
Q

What does streptococcus equi cause?

A

Causes strangles in horses. Purulent nasal discharge and abscesses in the lymph nodes of the head and neck
Can become systemic –> lymph to lungs, abdomen, brain

136
Q

What lansfield group is streptococcus pyogenes?

A

A

137
Q

What lansfield group is streptococcus equi?

A

C

138
Q

What is the iron binding siderophore of streptococcus equi called?

A

Equibactin

139
Q

What causes the black plague?

A

Yersinia pestis

140
Q

How does Yersinia pestis spread through the body?

A 
Flea bites skin
Lymphatics
Lymph nodes (enlarges - buboes)
Blood stream 
Lung (pneumonic plague)
Meningitis
Septicaemia
Multi-organ failure
141
Q

What are the virulence factors of Yersinia pestis?

A
  • Antiphagocytic capsule
  • Protein toxins including injected effector proteins called Yops that subvert mphage function to prevent engulfment
  • YopT  targets small GTPases to disrupt cytoskeleton
  • YopP  acetyltransferase inhibits signalling, triggering apoptosis
  • Inflammatory damage by LPS lipid A
142
Q

Pneumolysin

A

Enzyme secreted by streptococcus pneumonia
Resists removal by mucous and ciliated cells
Avoids phagocytosis
Causes lung damage

143
Q

How is tuberculosis caused by M Bovis controlled?

A

Widespread slaughter of infected cattle

Pasteurisation

144
Q

Why might control of M Bovis not work by slaughter?

A

Could be animal reservoir of badgers

145
Q

Why is mycobacterium TB called acid fast?

A

Difficult to destain with Gram stain due to mycolic acid waxy impermeable cell envelope

146
Q

What type of bacterium is mycobacterium Tb?

A

Obligate anaerobe

Grows slowly

147
Q

How does mycobacterium TB spread?

A

Small droplets

148
Q

How does mycobacterium TB survive in macrophages?

A

Establish a safe uptake pathway where they arrest trafficking and inhibit phagosome-lysosome fusion

149
Q

What is the pore forming toxin of mycobacterium TB? What does it do?

A

ESAT6 interferes with macrophage signalling pathways, so ROS downregulated

150
Q

What is the test for mycobacterial infection?

A

Tuberculin skin test

Inject mycobacterial protein –> CD4 Th1 –> IFNgama –> macrophages –> TNFalpha –> red, swelling.

151
Q

What happens when M. tuberculosis persists?

A

Swap from Th1 to Th2 response
Type IV granulomatous inflammation
Aggregates of activated mphages (may differentiate into epitheloid or multi-nucleate giant cells) surrounded by fibroblasts and a few lymphocytes ‘wall off’ the pathogen
Ongoing tissue destruction (necrosis) and repair (fibrosis, scarring)
Caseating granuloma

152
Q

What can result in a BoNT intoxication?

A

Home canned food

153
Q

What do you eat to get staph aureus food intoxication?

A

Custard, processed meats at room temperature

154
Q

How does cholera toxin work?

A
  • B binds to host receptor GM1-ganglioside
  • Receptor mediated endocytosis
  • Retrograde transport to ER
  • A translocates to host cell cytosol
  • A ADP-ribosylates the stimulatory Gs protein (GTP-hydrolysing), fixes in on state
  • AC levels elevated
  • Uncontrolled high levels of cAMP
  • Disturbs CFTR (Cl-) and Na+ membrane pumps
  • Water/electrolyte loss up to 20l a day
  • Copious rice water diarrhoea
  • Shock collapse, sometimes cardiac failure
155
Q

What is the subunit composition of CTX?

A

AB5

156
Q

Does salmonella typhi have an animal reservoir?

A

No

157
Q

What mediates the symptoms of salmonella typhi?

A

Typhoid toxin CDT cleave DNA (cytolethal distending toxin)

158
Q

How do you test for intestinal bacteria?

A

MacConkey agar - has bile salts in

159
Q

Is salmonella lac+ or -?

A

-

160
Q

Is E coli lac + or -?

A

+

161
Q

What is the toxin of ETEC?

A

LT labile toxin

ADP-ribosylates regulators of AC, disturb cAMP signalling and ion balance

162
Q

What type of E. Coli is 0157 serotype?

A

Enterohermorrhagic

163
Q

What is the toxin of EHEC?

A

Shinga like toxin

N-glycosidase that depurinates 28S rRNA so blocks protein synthesis

164
Q

Why is listeria such a problem?

A

Can become systemic: can cross placenta, and BBB (meningitis)

165
Q

When does C diff invade the colon?

A

After antibiotic eradication of the normal human gut microflora

166
Q

What are the C diff toxins?

A

TcdA TcdB
Glycosylate small GTPases in intracellular signalling pathways – subversion of actin cytoskeleton and disruption of tight junctions. Epithelium leak, cell destruction

167
Q

How do you treat C diff infection?

A

Vancomycin and rehydration therapy

Recurrent infections faecal transplants

168
Q

How and where does helicobacter pylori colonise the gut?

A
  • Colonises mucin layer near gastic mucosal cells in gastric antrum
  • Neutralises acid by urease, which also makes gastric mucous less viscous, which along with the highly motile flagellum makes it easy for helicobacter to swim towards the epithelium
169
Q

Which cytokine is associated with H pylori infection?

A

IL8 released by epithelial cells

Neutrophil chemotaxis

170
Q

What toxin does H pylori secrete and what does it do?

A

VacA – pore-forming vacuolating. Inserts into host cell membrane, anion selective channels, endocytosed, pore disturbs ion balance in late endosomes, water flows in, swells to form characteristic vacuoles. Induces apoptosis

171
Q

What is the structure of the VacA toxin?

A

Hexameric

172
Q

What is CagA?

A

H pylori

CagA bacterial effector also interferes with signalling pathways, leading to increased cell proliferation

173
Q

What mechanism may link H pylori to gastric cancer?

A

Chronic inflammation exposes proliferating mucosal stem cells to dietary carcinogens + generates mutagenic ROS
CagA bacterial effector also interferes with signalling pathways, leading to increased cell proliferation

174
Q

What are the forms of vaccination used against bacteria?

A
  1. Killed
  2. Live attenuated
  3. Subunit - toxin, adhesins, caspules (to block colonisation or toxin binding to receptors)
175
Q

Which vaccine is used against diphtheria?

A

Toxoid DPT

176
Q

Which vaccine is used against tetanus?

A

Toxoid DPT

177
Q

Which vaccine is used against whooping cough?

A

Killed bordetella pertussis DPT

178
Q

Which vaccine is used against pneumonia?

A

Polysaccharide from S pneumonia, H influenzae (subunit)

179
Q

Which vaccine is used against meningitis?

A

Purified polysaccharide from Neisseria meningitides

Capsular polysaccharide of Hib coupled to tetanus toxin (carrier)

180
Q

Which vaccine is used against cholera?

A

Killed whole cell or crude fraction of vibrio cholerae

181
Q

Which vaccine is used against tuberculosis?

A

BCG, attenuated strain of mycobacterium bovis

182
Q

Which vaccine is used against typhoid fever?

A

Live attenuated Ty21A

Vi capsular polysaccharide

183
Q

How do bacteria counteract penicillins?

A
  • Enzyme-mediated inactivation: beta lactamases break open the lactam ring
184
Q

How do bacteria counteract chloramphenicol and aminoglycosides?

A
  • Enzyme-mediated inactivation: produce acetyltransferases that modify chloramphenicol and aminoglycosides to prevent ribosomes from binding
185
Q

How do bacteria counteract tetracycline?

A
  • Alteration of target: some resistant bacteria produce ribosomal protection proteins that have structural similarity to translation elongation factors. Dislodge tetracycline from ribosome.
186
Q

How do bacteria counteract fluoroquinolones like ciprofloxacin?

A
  • R plasmid encoded quinolone resistance protein Qnr binds topoisomerase to physically block binding of the antibiotic
187
Q

How do bacteria counteract vancomycin?

A
  • Resistant gram + pathogens produce different peptidoglycan enzymes that synthesise D-Ala-D-Lac alternative peptide crosslinks
188
Q

What are the different mechanisms to counteract antibiotics?

A
  1. Enzyme mediated inactivation
  2. Alteration of target
  3. Metabolic bypass
  4. Efflux pumps
189
Q

How do bacteria counteract trimethoprim and sulphonamide?

A
  • Metabolic bypass: for both trimethoprim and sulphonamides. R-plasmid encoded DHPS and DHFR have a much lower binding affinity for the antibiotics than the normal bacterial enzymes.
190
Q

What is TolC?

A

An efflux pump which conveys multidrug resistance to gram -ve bacteria

191
Q

What is the structure of an efflux pump?

A

Drugs bind to inner membrane transporter (ATPase or proton antiporter), ejected through TolC exit duct spanning the periplasm and outer membrane (this is tripartite)

192
Q

How do we counteract increasing drug resistance?

A
  1. Selective antibiotic use to minimise selective pressure
  2. Develop new antibiotics against different targets (e.g. against lipid A synthesis, bacterial cell division, efflux pumps)
  3. Develop new antibiotics against pathogen-specific processes (quorum sensing signals, adhesion assembly)
  4. Combination therapies
  5. Use antibiotic potentiators e.g. clavulanic acid that inhibit resistance enzymes
193
Q

Name the obligate aerobes

A

P aeruginosa
Corynebacterium diphtheria
Neisseria pharynges

194
Q

How do superantigens work?

A

Bridges weakly interacting MHC Class II and TCR by binding outside the normal Ag-binding pocket. Activates useless T cells by promoting tighter binding and stronger signalling. Results in cytokine storm (IL1,2,TNF). Diverts T cell function.

BOD MVST 1b (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions