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BIOSCI 349 > Bacteriology > Flashcards

Bacteriology Flashcards

1
Q

Endotoxins - General Information

A

Cell-bound - released from bacteria as a result of cell lysis
LPS
LTA
Neisseria Lipooligosaccharide (LOS)

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2
Q

Exotoxins - General Information

A

Secreted
Soluble
Large Variety

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3
Q

Endotoxins - What does it bind to?

A

LPS/LTA bind to CD14 and TLR-4 on APC, initiates a very strong pro-inflammatory cytokine response through to increase of NFkB promotor which induces transcription of inflammatory cytokines. Can lead to septic shock

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4
Q

Types of Bacterial Exotoxins

A

Membrane-damaging toxins
Intracellular toxins
Toxins that act from the cell surface
Toxins that interfere with the immune response

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5
Q

Subset of Membrane-damaging toxins

A

Pore-forming toxins
Toxins that enzymatically damage the membrane
Toxins with detergent like effect

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6
Q

Subset of Intracellular toxins

A

AB toxins (large group)
Injected toxins (Type III and IV secretion)

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7
Q

Subset of toxins that act from the cell surface

A

Superantigens

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8
Q

Subset of toxins that interfere with the immune response

A

Complement inhibitors, Ig- proteases

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9
Q

Pore-forming Toxins - General info

A

Secreted by bacteria (mainly Gram-positives) as soluble monomers
Oligmerisation within the host membrane
Central channel (pore)

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10
Q

Classes of PFT

A

alpha-PFTs - Colicins, P.aeruginosa exotoxin A

beta-PFTs - alpha hemolysin (S.aureus), Cholesterol-dependent cytolysins (CDCs)

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11
Q

beta-PFTs: General info

A

Pore is build by beta-stand domains
Transition from water-soluble to amphipathic B-barrel (membrane pore)
Use certain host proteins as receptors
Oligomers from voltage gated channels
Permeation of water, ions and small organic molecules
Can lead to osmotic lysis of the cell and eventual cell death
Hydrophillic on inside, hydrophobic on outside

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12
Q

beta-PFTs - CDCs: General info

A

Secreted as monomers by certain Gram+
Insert as pre-pore complex
Adding more monomers to pre-pore to make into pore
E.g Pneumolysin

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13
Q

PFTs - Clinical Relevance
Pneumolysin - Cholesterol-depedent PFT

A

Mutants pneumococci deficient in pneumolysin are cleared from lungs
Neutralising antibodies against pneumolysin protects mice from PC challenge
Pneumolysin destroys ciliated epithelial cells and phagocytes
Cytolytic activity increases neutrophil infiltration into lungs (inflammation)
Pneumolysin is an essential virulence factor for development of pneumonia
Pneumolysin can also induce inflammation in brain, if bacteria breach BBB and colonise CSF

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14
Q

Cytolysins with Enzymatic Activity

A

Clostridium perfringens alpha toxins - Zn- metallophospholipase C

Low conc - limited hydrolysis of PC, generation of DAG -> leading to apoptosis, signal transduction pathways

High conc - massive degradation of PC, membrane disruption, cell lysis

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15
Q

C.perfringens alpha toxin and disease

A

Targets erythrocytes, platelets, leukocytes and epithelial cells
Damage of cell membrane results in release of secondary messengers
IP3 initiates Ca2+ influx
Increased vascular permeability, edema
tissue destruction (clostridial myonecrosis, gas gangrene)

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16
Q

Membrane-damaging toxins - functional relevance

A

Nutrition
Iron is essential for the growth of many pathogens
Free iron is only found at very low concentration in blood (can form damaging free radicals)
Erythrocyte contain plenty of iron

Spreading
Tissue destruction allows bacteria to spread and colonise other tissue

Immune Evasion
Destruction of immune cells
Listeriolysin lyses phagosome (enables Listeria to live in cytosol of host phagocytic cells)

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17
Q

AB toxin (Binary toxins)

A

B-subunit attaches to target regions on cell membranes (receptor - binding)
A-subunit possesses enzymatic activity that affects internal cellular bio-mechanisms

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18
Q

A and B domains

A

Clostridial neurotoxins, diphtheria toxin, large clostridial toxins

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19
Q

AB5 toxin

A

E.g Cholera toxin, pertussis toxin, shiga toxin

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20
Q

Uptake and trafficking of AB toxins

A

See diagram in lecture slides

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21
Q

How to AB toxins work?

A

-B subunit attaches to target regions on cell membranes (receptor binding)
-AB complex enters through the membrane by endocytosis
-A possesses enzymatic activity that affects internal cellular bio-mechanisms

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22
Q

Most common intracellular target for A-subunit

A

Elongation factor 2- stop protein production
G proteins
Rho proteins
Actin
Nucleus
28s rRNA

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23
Q

Enzymatic activity of CT and LT subunit A

A

-‘A’ subunit is a globular enzyme that ADP ribosylates Ga of stimulating G proteins
- constant activation of cyclase
-increased levels of cAMP
- activation of protein kinase A
-PKA phosphorylates CTFR and causes active Cl- secretion
-massive efflux of electrolytes and fluids
-CT: fluid loss from intestine: 500 - 1000 ml/h (up to 40L per day)

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24
Q

CT (cholera toxin)

A

-Produced by Vibrio cholerae carrying lysogenic phase
-infection from contaminated food and water
-Vibrio colonises gastrointestinal tract causing infectious gastroenteritis
- extensive diarrhea
-epidemic outbreaks

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25
Q

Heat-labile enterotoxin (LT)

A

-produced by enterotoxigenic E.coli (ETEC)
-plasmid encoded
-LT induced diarrhea usually less sever than CT diarrhea
-traveler disease

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26
Q

Injected Toxins - which species?
Read on secretion systems

A

Salmonella spp
Shigella spp
Yersinia spp
E.coli

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27
Q

Salmonella typhimurium effector proteins

A

Salmonella invasion proteins (SipA and C)
-act directly and cooperatively on actin, mediate bundling and polymerisation
-SipA acts a molecular staper
-SipC promotes actin nucleation and filament bundling

Salmonella outer protein (SopE)
-mimics the function of G nucleotide exchange factor (GEF)
-activation of small G proteins of the Rho family
-actin nucleation and branching causing membrane ruffling*

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28
Q

Which genera have superantigens?

A

Staphylococcus
Streptococcus
Yersinia
Mycoplasma

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29
Q

Superantigens: General info

A

-very powerful T cell mitogens
-SAgs bind to MHCII outside the antigen binding groove and to the TcR VB chain
-overstimulation of T cells (up to 20% of the total population)
-massive release of pro-inflammatory cytokines (IL-1, TNF-a, IFN-y)
-can induce shock like conditions in animals
-relevance disease not fully established
-likely to be involved in staph/strep toxic shock syndrome possibly in combination with endotoxins (synergistic effect)
-bacteria enter blood through wounds,small cuts
-superantigens play important role
-cytokine storm leads to systemic inflammation

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30
Q

Antimicrobial host factor - charge? and what are they?

A

Positive
-antimicrobial peptides
-lactoferrin
-lysozyme
-myeloperoxidase

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31
Q

Bacterial cell envelope - charge? and what are they?

A

Negative
-peptidoglycan (PG)
-teichoic acids (TA)
-lipoteichoic acid (LTA)
-lipid A
-LPS

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32
Q

4 CAMP resistance mechanisms

A

Repulsion of CAMP
Extrusion of CAMP
Neutralisation of CAMP
Cleavage of CAMP

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33
Q

Repulsion of CAMP - mechanism

A

Modification of TA or lipid A (Staph,Strep)

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34
Q

Extrusion of CAMP - mechanism

A

MtrCDE efflux pump
(Neisseria)

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35
Q

Neutralisation of CAMP - mechanism

A

Staphylokinase, SIC
(Staph,Strep)

36
Q

Cleavage of CAMP

A

PgtE proteases
(E.coli, Salmonella)

37
Q

Ways in which bacteria evade complement

A
  1. Modulation or inhibition of complement proteins
  2. Inactivation by enzymatic degradation
  3. Recruitment or mimicking of complement regulators
38
Q

Modulation or inhibition of complement proteins - mechanism

A

Staphylococcal complement inhibitor (SCIN)
- binds to C3 convertases
- inhibits C3 activation

Streptococcal inhibitor of complement (SIC)
- binds to C5b-C7/C8
-Prevents formation of MAC

Staphylococcal protein A
-on bacterial cell surface
-binds Fc region of IgG
- prevents opsonisation and classical pathway

Chemotaxis inhibitory protein of Staph aureus (CHIP)
- binds to C5a receptor
-inhibits C5a signalling

39
Q

Inactivation by enzymatic degradation - mechanism

A

Pseudomonas proteases
- cleave C3
- prevent C3b opsonisation

Pseudomonas elastase
-cleaves IgG and C1q
-prevents initiation of classical pathway

C5a peptidase
-cleaves C5a
-prevents neutrophil chemotaxis

40
Q

Recruitment and Activation of Plasminogen (Staphylokinase + Streptokinase)

A

Enzymatic conversion of plasminogen to plasmin. Plasmin cleaves IgG, C3b and dissolves blood clots

41
Q

Recruitment or mimicking of complement regulators

A

C4 binding protein
- acceleration decay C3 convertases
-recruited by Streptococcus, E.coli
Haemophilus influenza, Moraxella catarrhalis, Neisseria gonorrhoe (porin)

Factor H (FH)
-degrades C3b
-accelerates decay of AP C3 convertases
-recruited by Streptococcus (M protein)
-Haemophilus influenza

42
Q

DNases as immune evasion factors

A

DNA + antibacterial protein (histones, elastases) = Neutrophil extracellular trap (NET)

43
Q

Role of LPS in Immune Evasion

A

Modification of LPS with sialic acid
- FH prevents opsonisation of sialic acid-containing surfaces
-many strains of Neisseria spp are ‘serum resistant’ - because complement pathway inhibited

Long side chains
- physically interact with how phagocyte and C3b interact

44
Q

Protective capsules

A

Polysaccharide: Antigenic variation, serotypes

Hyaluronic acid:
Streptococcus pyogenes “camouflauge”
-see diagram

45
Q

Phagocyte evasion by bacteria

A

Block proton pump preventing acidification - cytolysin

Block lysosome fusion (cell wall)
Arrest phagosome maturation - TB

Phenolic glycolipid - prevents reactive oxidative intermediates entering phagosome

Catalase - breaks down hydrogen peroxide

46
Q

Invasion of non-phagocytic cells: General info

A

-Shelter from antibodies, complement, antibiotics
-Uptake has to be induced by bacteria
-Requires extensive reorganisation of actin cytoskeleton
-Some bacteria inject toxins (effectors)
-Type III secretion system (T3SS)
- E.coli, Shigella, Salmonella
- intracellular replication

47
Q

Biofilms - another place to ….

A

hide

48
Q

Antigenic variation

A

Due to genetic (allelic) variation, microorganisms are often able to change epitopes in proteins or carbohydrates. eg adhesins, pili, flagella

Leads to relapsing infections

49
Q

Why in vivo models?

A

Explore mechanisms of microbial pathogenicity
Explore mechanisms of host immune response
Find new approaches to the treatment of infections
Find new targets for vaccine development
Estimating efficacy/tolerability of a treatment/vaccine before administration to humans

50
Q

Ideal features of a model

A

Identical/very similar:
Causative agent
Route of entry
Spread in body

Amenable to analysis (measurable, predictable, reproducible)
Tissue involvement
Severity
Course and duration of disease

51
Q

3 R’s Ethical responsibilities

A

Replacement, Refinement, Reduction

52
Q

C.elegans - general info

A

-Feed on non-pathogenic E.coli so can be fed other microorganisms
-Bacteria pass through pharyngeal grinder and into the digestive tract
-Bacteria establish in appropriate niche
-Innate immune response triggered
-Worms or eggs placed on petri-dish with lawn of bugs to be tested
-Examined at 24h intervals
-Considered dead if do not respond to prod or shaking of petri-dish

53
Q

Drosophila melanogaster - general info

A

-Infection by septic injury or injection of bacteria directly into the abdomen or hemocoel
-Injury alone can cause stress and death
-Can use both KO hosts and microbes

54
Q

Danio rerio

A

-Tropical freshwater fish AKA zebrafish
-Omnivorous
-Well developed immune systems
-Causes locally spreading necrotic disease confined to muscle
-No recruitment of inflammatory cells
-Useful for developmental disease
-KO mutants and fluorescent cells available

55
Q

Galleria mellonella

A

-Greater wax moth/ honeycomb moth
-Use the larvae (=wax worms)
-Inject by injection the plug
-Can survive incubation at 37C
Well developed innate immune system

56
Q

Mus musculus

A

-Many different strains
-Disease relies on species-specific interactions (microbial ligands and host receptors)

57
Q

Humanised mice

A

-Developed transgenic mice containing human E-cadherin

58
Q

Specialised pathogens

A

When a pathogen colonises an animal body the same way another pathogen colonised the human body

59
Q

Biophotonic imaging

A

Non-invasive, non-destructive, real-time technique for measuring light based on fact that light travels through flesh and skin

60
Q

Advantages and Disadvantages of all animals

A

See table in lecture slides

61
Q

Drugs that block cell water synthesis: B-lactam antibiotics

A

inhibit peptidoglycan synthesis by irreversible inhibition of transpeptidase (=penicillin binding protein PBP), the enzyme that catalyse the peptide-cross links. Eg. penicillin. These antibiotics are bactericidal

B-lactams include penicillin, cephalosporins, carbapenems

Gram negative bacteria are resistant to penicllin, does not pass through outer membrane porins, however extended spectrum penicillins (amoxicillin, ampicillin) can

62
Q

Drugs that block cell wall synthesis: Glycopeptides

A

which inhibits PG synthesis by binding to the petides of the peptidoglycan monomers. Drug of last resort for MRSA. eg vancomysin

63
Q

Inhibitors of RNA transcription: Rifamycins

A

inhibit bacterical RNA polymerase. typically used against Myobacteria. Rifamysins are bactericidal.

64
Q

Inhibitors of nucleic acid synthesis: Quinolones and Fluoroquinones

A

bind DNA topoisomerases and prevent DNA replication. They are broad spectrum, bactericidal and coomnly used against urinnary tract infection. They can enter host cells, which makes them useful against intracellular bacteria. Due to increased resistance, quinolones have been replaced with fluroquinolones which are more active.

65
Q

Antimetabolites: Sulfonamides and diaminopyrimidines

A

prevent the synthesis of tetrahydrofolic acid from PABA. Tetrrahydrofolic acid is a cofactor needed to synthesise nucleic acids and methionine. Mammalian cells depends on external folate. These antibiotics are bacteriostatic and useuful against urinary tract infection and Shigellosis

66
Q

Antibiotics: Inhibition of protein synthesis

A

Antibiotics that can bind to the 2 different subunits of the ribosomes, some targeted to the 50s and others to the 80s.

67
Q

Binding to the 30s subunit: Aminoglycosides

A

freeze the 30s initiation complex resulting in misreading (induce frameshift) of DNA. They are mostly effective against aerobic, gram negative bacteria and are bactericidal and synergistic with penicillin.

68
Q

Binding to the 30s subunit: Tetracyclines

A

inhibit binding of aminoacyl-t-RNA to the acceptor site on the ribosome. They have broad-spectrum activity, are bacteriostatic and used against many different bacterial infections.

69
Q

Binding to the 50s subunit: Macrolides

A

inhibit translocation of the peptidyl transferase activity. from the A to the P site. They are bacteriostatic and active against Gram-positives and Mycoplasma

70
Q

Binding to the 50s subunit: Lincosamides

A

inhibit peptidyl transferase activity. They have broad-spectrum activity and are bacteriostatic

71
Q

Binding to the 50s subunit: Chloramphenicol

A

is a broad-spectrum, bacteriostatic antibiotic. Only used in certain cases such as bacterial meningitis, due to strong side-effects

72
Q

Antibiotic resistance mechanisms

A

Exclusion of antibiotic from site of action - outer membrane of Gram-negatives often impermeable

New or modified antibiotic insensitive target - MRSA produces PBP2a (altered transpeptidase) with reduced affinity for penicillin

Efflux pump for the antibiotic removal from site of action - specific transport out of the cell e.g tetracylclin, macrolides, fluroquinolones

Enzymatic modification or degradation of the antibiotic - some bacteria produce B-lactamase, which breaks the B-lactam ring. Some B-lactamases are specific for certain B-lactams, while others inactivate a wide range of B-lactams.

73
Q

Antibiotic resistance (genetic vs non-genetic)

A

Non-genetic (intrinsic drug resistance

  • metabolic inactivity
  • lack of target structure, mycoplasmas (lack cell wall)
  • exclusion, antibiotic can’t enter cell

Genetic resistance

  • Chromosomal resistance- spontaneous mutation n a gene encoding a target receptor
  • Acquired resistance - conjugation (plasmid transmid)
  • Transformation (transfer of free DNA)
  • Transduction (Transfer by viral DNA)
74
Q

MRSA

A

Methicillin resistant S-aureus, carry Staph cassette chromosome mec (SCCmec)
integrated in bacterial genome
SCCmecII: mainly in hospital MRSA strains, also encodes resistance
SCCmecIV: mainly in community acquired MRSA

75
Q

Selective Agar

A

Contains inhibitors to discourage growth of certain organsism

76
Q

Differential Agar

A

Contains indicators to differentiate organisms.

77
Q

Mannitol Salt Agar

A

use to identify Staph aureus. Salt inhibits non-haloduric bacteria, mannitol can be used as a carbon source by Staph aureus, but not by an other Staphylococci. Fermentation of mannitol results in a pH decrease, which is detected by a pH indicator changed from red to yellow

78
Q

Sabourand agar

A

selective for fungi, as low pH suppresses growth of most bacteria. Non -differential

79
Q

Eosin-methylene blue agar (EMB)

A

selective for gram-negative bacteria as aniline dyes are toxic for gram positive bacteria. Differential for lactose fermenter. Appearance fo pink colonies indicates lactose fermentation (white = negative)

80
Q

Blood Agar plate

A

Growth of many fastidious bacteria. Differentiates for haemolytic reactions. alpha = some, beta = all, gamma = none

81
Q

Cytine-lactose-electrolyte deficient (CLED) agar

A

used for growth of urinary pathogens. Lack of electrolytes inhibits movement of motile organisms. Differentiates lactose fermenters (yellow), blue = negative

82
Q

Bile-Esculine agar:

A

selective for Enterococci (Group D streptococci). Oxgall inhibits non-enteric bacteria. Esculine hydrolysis results in a dark brown color. Some members of the Enterobacteriaceae family also hydrolyse esculine

83
Q

Obligate aerobes

A

Required O2, no fermentation, e.g mycobacterium tuberculosis

84
Q

Obligate anaerobes

A

cannt survive in presence of oxygen (e.g clostridium tetani)

85
Q

Facultative anaerobes

A

can metabolise energy aerobically (respiration) or anaerobically (fermentation). Prefer O2 as more ATP is produced, e.g E.coli

86
Q

Microaerophiles

A

Require oxygen (no fermentation), but cannot survive in higher concentrations of O2 (e.g Helicobacter pylori)

87
Q

Aerotolerant bacteria

A

cannot ulilise O2 (fermentation only) but are not harmed

BIOSCI 349 (5 decks)

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