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Bacteriology Flashcards

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1
Q

Detail the ways that streptococcus pyrogenes attacks and evades the immune system:

A

Evasion:
- Capsule
Inhibition:
- Inhibit chemotaxis by cleavage of C5a
- Superantigenic pyrogenic toxins
- M protein on surface binds complement factor H to C3b

Attack:
- Pore-forming toxins = Streptolysin O and S
- Hyaluronidase = breaks down tissue
- Streptokinase = lyses clots
- DNAse = depolymerises DNA in pus

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2
Q

What are Koch’s Postulates and how was it shown?

A

Specific bacteria causes specific disease

  • Bacterium present in every case of disease
  • Bacterium isolated from disease and grown in pure culture
  • Specific disease reproduced from pure culture in healthy host
  • Bacterium recovered again
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3
Q

What are the different ways that bacteria can be transmitted?

A

Horizontal transfer:
- Sexual contact
- Respiratory tract (TB, pretussas)
- Contamination from one body part to another
- Contact with skin and eyes

Vertical transmission:
- Transplacental or during parturition

Indirect contact:
- Contamination with water, soil, food, animals…

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4
Q

How has bacteriology helped the progression of biology?

A

Fundamentals of genetics and genetic manipulation:
- Gene regulators; transcription; translation
- Restriction enzymes; plasmids; ligases; polymerases
- Gene editing (CRISPR/cas9)

Host biology insights:
- Intracellular trafficking; innate immunity; cell motility; signal transduction

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5
Q

Describe the surface structure of gram +ve bacteria:

A
  • Thicker peptidoglycan wall of alternating NAM and NAG residues
  • Cross linked with oligopeptides
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6
Q

Which bacteria do not gram stain? Why?

A

Chlamydia and mycoplasma lack major cell wall.
- Mycobacterium are acid-fast (hard to stain due to waxy coat)
- Stain instead with Ziehl-Neelsen

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7
Q

Describe the surface structure of gram -ve bacteria:

A
  • Thinner peptidoglycan wall with periplasm between two membrane layers
  • Outer membrane is atypical: contains porins for transport and lipopolysaccharides
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8
Q

What are some uses of LPS on bacterial surfaces (both for the bacteria and for the host)

A
  • O-ring of LPS highly variable (many antigen serotypes) and resists complement by stochastic resistance
  • Lipid A of LPS is endotoxin released from dying bacteria = a PAMP for TLR4
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9
Q

How to bacteria transport molecules across their surface?

A
  • Porins on outer surface (inserted by BAM)
  • Toxin seretion through ToIC exit duct

Standard secretion pathway (sec):
- Exports molecules with N-terminal export signal (ATPase powered)
- Using SecYEG
- Significant for pili and adhesin molecules.

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10
Q

What are the benefits of a capsule and how can it be identified?

A
  • Prevents drying out
  • Protects against complement and macrophages
  • identified using charged stain (e.g. Congo red)
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11
Q

What are some molecules forming the bacterial cytoskeleton?

A

Rudimentary cytoskeleton: controls cell shape:
- MreB (actin homologue)
- FtsZ (tubulin homologue - creates central rings during cell division)
- Crescentin in crescent bacteria threads through MreB/FtsZ

Coordination between peptidoglycan and MreB to assemble/disassemble

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12
Q

How is genetic material organised in a bacterium to increase metabolic rate?

A

Central loop and plasmids (100-9000 genes possible):
- Coupled genes (operons)
- Coupled transcription-translation mRNA (often polycistronic (read from multiple genes))
- Rapid mRNA and protein turnover

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13
Q

How can genes and gene expression change in bacteria?

A

Gene expression alteration:
- Local environment (e.g. chemotaxis)
- Quorum sensing

Genome evolution:
- Insertion sequences (IS) causing recombination of own genes
- Transposons pick up genes; transposases recombine (e.g. new resistance gene)
- Genetic exchange mechanisms

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14
Q

Describe an example of quorum sensing:

A

Glutamate sensing in biofilm bacteria:
- Central bacteria lack glutamate
- In response, pump out K+ through YuGo channels
- High K+ in outer bacteria causes cession of glutamate intake, increasing diffusion into centre

Pseudomonas colonises lungs of cystic fibrosis patients using alginate polysaccharide

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15
Q

How do bacteria move?

A

Flagella (one or many):
- Made of flagellin
- Coordinated swimming (AntiCW)
- Tumbling (CW) for random motion
- Aids through mucus and for swarming

Pilli (e.g. Sex pilus for conjugation) or cell surface adhesins (on end of pili):
- P-pilus on uropathogenic E.coli which binds kidney receptor

Chemotaxis (sensation and transit information to motor):
- Alters gene expression

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16
Q

What are the stages of colonisation?

A

Find host (tropism):
- Motility helpful (e.g. H.Pylori)

Adhere to host:
- Tight adhesion using adhesins (E.g. K88 on ETEC)
- Adhesin on pillus to increase attachment probability
- Pedestal formation

Further colonisation:
- May rely on damage or changing cellular action

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17
Q

How do EPEC and EHEC form a pedestal?

A

Host cell induced to form a pedestal on which bacteria sits
- Injection of translocated intimin receptor (TIR) using injectosome needle
- TIR becomes a membrane receptor (on host side)
- Bacterial intimin receptor binds TIR (tight adhesion)
- Promotes actin polymerisation

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18
Q

What are two ways that bacteria induce non-phagocytic cells to engulf them?

A

ZIPPER mechanism: - Bacteria encode invasins which mimic host ligands
- Adhesin forms initial contact
- Triggers intracellular signalling
- Mimics cell attaching to a surface causing cytoskeletal rearrangement

TRIGGER mechanism: e.g. salmonella
- Same injection mechanism as pedestal formation but injects Sips and sops
- Cytoskeletal rearrangement

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19
Q

What are virulence genes? Include examples.

A
  • Often carried on plasmids/bacteriophages / grouped into pathogenicity islands (PAI)
  • Typically have a GC content different to surrounding DNA
  • Easier to spot than individual genes (often transferred as whole section)

E.g. Salmonella has SPI-1 and SPI-2 which determines entry to non-phagocytic cells or survival in macrophages by TRIGGER mechanism

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20
Q

How does UPEC cause disease?

A

Uropathogenic E.coli (UPEC) causing UTI:
- Swim up urethra and binds bladder cells using type 1 pili.
- Colonisation of kidneys by exposing P-pili instead.
- Damage caused by toxin
- Some UPEC can be endocytosed into cell
- Adhesin binds tighter with increased urine flow to wash it away
- UPEC endocytosed and colonise cell. Cell eventually dies

Chronic infection: Some bacteria go deeper into cell layers which can later resurge

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21
Q

Provide examples of secreted enzymes bacteria use to survive extracellularly:

A
  • Collagenase: breakdown connective tissue
  • Interfere with clotting: coagulase (fibrin clot formation)/Staphylokinase (dissolve blood clots)
  • DNase: to break down DNA in pus
  • Streptococcal C5a peptide: cleaves C5a to prevent MAC formation and macrophage chemotaxis
  • Antibody inactivation by protease degredation
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22
Q

How does listeria infect cells and spread?

A
  • Uptake induced via ZIPPER mechanism
  • Listeriolysin O used to escape vacuole
  • Develops actin comet tail to disrupt intracellular cytoskeleton (ActA on one end of bacterium)
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23
Q

Give examples of molecules used by bacteria to manipulate host cytoskeletons:

A
  • ActA on listeria –> actin comet tails formed
  • Glycosylating toxins (c.diff) modify GTPases
  • Deaminasing toxins (UPEC) necrotising factor deaminates GTPases
  • Salmonella injection of SipA/C/P (ZIPPER mechanism)
  • Salmonella SPI-2 effectors create F-actin mesh around SCVs in cytosol
  • C.diff TcdA/B toxins (GTPases) result in subverted cytoskeleton and tight junction disruption
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24
Q

Describe the lifecycle of chlamydia:

A

Obligate intracellular parasite (cycles between infectious elementary bodies and replicative reticulate bodies):
- EB induce membrane ruffling; attach and are taken-up into endosome (Tarp injected using virulence needle)
- EB differentiate into RB and endosome expands with RB replication inclusion body formed)
- RB differentiate back into EB and are released when host cell lyses

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25
Q

Describe the structure of Chlamydia and disease incurred:

A

Structure:
- Small genome (900 genes) = virus like
- Gram -ve with internal nucleoid and injectosome

Disease:
- Inflammation induced by LPS on surface
- Urethritis and infectious blindness (STI)
- Many asymptomatic carriers

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26
Q

What are some barriers to bacterial infection?

A

Physical:
- Skin = acidic, dry, high salt.
- Mucous membranes.

Chemical:
- Gastric acid and bile salts. - Lysozymes and iron limitation by lactoferrin and transferrin
- Resident microflora – inhibits colonisation by occupancy and generation of toxic waste

Immunity
- Innate: complement; inflammation; macrophages; PAMP recognition
- Adaptive: classical pathway of complement; Ig production; cell mediated immunity (CD8)

27
Q

How do bacteria protect themselves from chemical threats due to host defences? Give specific examples.

A

Iron scavenging:
- Reimportation of essential iron using siderophores (secreted and reimported)
- E.g. pyroverdin (green fluorescent) secreted by pseudomonas aeruginosa
- E.g. Equibactin

Resist low pH:
- Pump H+ out/produce NH3 through urease action (urea taken in; NH3 secreted to mop up protons)
- E.g. Shigella or Helicobacter

28
Q

How do bacteria attack macrophages? Give examples.

A

Prevent phagocytosis:
- E.g. Yersinia injection of YopT and YopP

Inhibit chemotaxis:
- Strep. pyrogenes cleave C5a (using peptide)

Resist uptake by shielding:
- Steric hindrance of LPS O and capsule
- Sialic acid as camouflage

Kill macrophage:
- Injected molecules (streptolysin S)
- Destroy membrane (streptolysin O creates pores)

29
Q

What are some ways that bacteria have adapted to live inside a macrophage?

A

Disrupt antigen presentation pathways:
- E.g. Salmonella. Typhi

Resist oxidative stress:
- E.g. mycobacterial waxy cell envelope deflects lysosomal enzymes

Build protective microenvironment:
- E.g. legionella: deflect replicative compartment from maturing into endolysosome

30
Q

What are some ways that bacteria reduce the efficacy of antibodies?

A

Evade recognition:
- Mimic host (E.g. Neisseria attach sialic acid to LPS O antigen end)
- Phase variation/DNA rearrangement of antigens
(E.g. Salmonella has two alternative flagellin forms (1 and 2); Neisseria generates variable adhesion pilin genes (silent alternative alleles))

Inactivate antibodies:
- Proteases degrade secreted antigens (IgA inactivation by s.pneumoniae)
- Binding of Fc region (prevents opsonisation)

31
Q

What are cytolysins and what do they do. Give examples.

A

Target cell membranes

Degrade phospholipid bilayer = Phospholipases
- Clostridium perfringens α-toxin

Pore formation: induces conductivity changes
- Strep. Pneumoniae = pneumolysin;
- Strep. Pyrogens = streptolysin O

Affected by concentration: high concentration = disrupt membrane
- Low concentration interrupts host cell signal transduction (HA and leukotriene release)

32
Q

Detail the different classes of bacterial toxins:

A
  • ADP-ribosylating (DTX/CTX)
  • Adenylate cyclase mimicking (b.anthrasis)
  • Glycosidases (EHEC)
  • Glycosylating toxins (c.difficile)
  • Genotoxins
  • Deaminases
  • Neurotoxins
33
Q

How does diphtheria DTX toxin act?

A

AB structure
1. B subunit binds HB-EGF
2. Host protease furin nicks DTX to leave it only connected by disulphide bridge.
3. Acidification (by V-ATPase) in endosome triggers B-dependent translocation of A across into cytosol.
4. Disulphide bridge reduced in cytosol, releasing A and blocking protein synthesis by ribosylating EF-2.

Colonisation of nasal epithelium (and DTX release) leads to inflammation and occlusion of airway by pseudo-membrane formation.

34
Q

How does Cholera CTX toxin act?

A

AB5 pentameric structure
1. B binds GM1-ganglioside
2. AB5 translocates to the nucleus (via ER retrograde transport)
3. A then short circuits AC by ribosylating Gs (fixes it ON leading to very high cAMP levels
4. CFTR (Na+/Cl+) pump action disrubed
5. Ion imbalance draws water into lumen = watery diarrhoea

35
Q

How do toxins produced by EHEC and clostridium difficile act?

A

EHEC: glycosidase toxin
- Depurinates 28s rRNA to block translation

C.Difficile: glycosylating toxin
- modifies small GTPases to disrupt signalling/cytoskeleton

36
Q

How might extracellular conditions alter the production of DTX by diphtheria?

A
  • DTX genes carried on bacteriophage integrated into genome.
  • Controlled by TF DtxR
  • Represses gene expression when bound to Fe
  • So low iron increases DTX secretion
37
Q

How have bacteriophages influenced bacterial infectivity?

A

Allow large transfer of genes such as pathogenicity islands inherited together:
- CTX genes integrated as such and regulated with adhesin by a HAP transduction system
- DTX also PAI; controlled by TF DtxR (represses gene expression in high Fe)

38
Q

Describe the mode of action of two named neurotoxins:

A

Tetanus (TeNT):
- Made during anaerobic growth
- B chain binds receptor on pre-synaptic membrane
- A chain cleaves synaptobrevin in inhibitory neurons
- Spastic paralysis in CNS

Botox:
- B chain binds to receptor on pre-synaptic membrane
- A chain cleaves SNAP-25; blocking vesicle docking/release
- Leads to flaccid paralysis

38
Q

What are superantigens?

A
  • Weakly interact with MHC II and TCR by binding outside binding groove
  • Actives useless T cells resulting in cytokine storm
  • IL1; IL2; TNF (diversion of T cells to random targets)

E.g. Toxic shock syndrome; staph. aureus and strep. pyrogenes

39
Q

What are the ways that indirect damage can occur due to host response?

A
  • Wrong place (e.g. LPS crossing BBB causing meningitis)
  • Too long (chronic disease such as H.Pylori/TB
  • Too much (sepsis, toxic shock or deposition of immune complexes (E.g. borrelia in Lyme disease)
  • Autoimmune disease (hypersensitivity III) E.g. streptococcal M protein cross reactivity causing rheumatic fever.
40
Q

How does Yersinia Pestis colonise and cause disease?

A
  • Spread to lymphatics can lead to plague; septicaemia; necrotic tissue and death.
  • Extracellular bacterium
  • Remains infectious after death (person to person transmission – bypass flea vector)

Virulence factors:
- Anti-phagocytic capsule
- LPS A and injected effector proteins:
YopT inhibits GTPase; YopP inhibits Nf-kB pathway

41
Q

How does streptococcus pneumoniae colonise and cause disease?

A

Causes pneumonia

  • Colonises nasopharynx (using adhesin)
  • Resists mucous/ciliated cells using pneumolysin and IgA proteases.
  • Resists phagocytosis using pneumolysin and polysaccharide capsule (prevents opsonisation)
42
Q

How does bordetella pertussis colonise and cause disease?

A

Causes whooping cough

  • Aerosol inhalation and colonisation (using adhesins)
  • Damage caused by LPS A (inflammation induced) as well as secreted toxins (pertussis toxin (AB toxin) and adenylate cyclase)
  • Diphtheria-pertussis-tetanus vaccine effective for DPT.
43
Q

How does tuberculosis colonise and cause disease?

A

Non-motile obligate aerobe
1. Spread in small droplets
2. Ingested by alveolar M1 macrophages/DCs
3. Resists killing by establishing ‘safe uptake’ pathway preventing phagolysosomal fusion
4. Lyses host cell using ESAT6 proteins (downregulates ROS)
5. Some bacteria disseminate into lymph nodes
6. Can lead to granuloma formation/caseous necrosis and miliary TB

44
Q

How does the immune system react against TB?

A
  • Macrophages activate CD4+/Th1 cells which in turn activate macrophages (IFNγ)
  • This increases efficacy of killing (NO etc upregulated)
  • Balance between inflammation (risk direct damage) and bacterial burden
  • Granuloma formation (can later lead to miliary TB (dissemination)/caseous necrosis)
45
Q

How can bacteria cause disease without colonisation?

A

Food intoxications = poisonings without colonisation (toxin causes illness)
- Clostridium botulinum: botox (BoNT) produced during anaerobic growth.
- Staphylococcus aureus: stable enterotoxins interact with gastric mucosa
- Clostridium perfringens: germinates from spores in the environment

46
Q

How does salmonella cause disease?

A
  • ZIPPER mechanism ingestion (inject SipA/C/P using SPI-1 encoded needle)
  • Prevention of vacuole fusion using second injection system
  • Nutrient gathering using projections out of vacuole
  • Replicative niche formed in vacuole
  • Taken up by macrophages
  • Resist death using SPI-2 genes
47
Q

How do SPI-2 genes help salmonella to survive in a macrophage?

A
  • Resist defensins
  • Resist oxidative bursts using superoxide dismutase, catalase and pumps
  • Expression of mCAT channel to increase amino acid uptake into vacuole
48
Q

How does E.Coli cause diarrhoeal disease?

A

ETEC:
- Colonises using fimbrial pili adhesins
- Labile toxin (CTX-like)

EPEC:
- Attach by pilus adhesin
- Forms pedestals (including effacement pedestals (reduction in microvilli))
- Pedestals can move around and spread between cells.

EHEC: attach by pilus and pedestal formation (like EPEC)
- Inflammation due to shiga-like toxin (SLT) causing renal failure. E.g. O157 in beef

49
Q

What principles are used to combat bacterial disease?

A

Reducing exposure:
- Control of infection sources (clean water; cooking food)
- Reduce transmission

Reducing susceptibility:
- Vaccination

Reduce lethality:
- Antibiotics
- Antibacterial agents

50
Q

What are the different vaccination types used to combat bacterial disease?

A

Attenuated or dead bacteria:
- BCG for TB (attenuated)
- Ty21A for typhoid fever (attenuated)
- DPT for whooping cough (dead)

Genetically engineered:
- V.cholerae with the gene for toxin deleted entirely
- Utilise injection mechanism of to deliver antigens (not toxins) (E.g. salmonella)
- mRNA vaccines

Toxoid vaccines:
- Included in Diphtheria-Pertussis-tetanus (DPT) vaccine

Subunit vaccines:
- Against capsules

51
Q

What principles to antibiotics exploit to target bacterial disease?

A

Difference between host and bacteria in:
- Sensitivity to drug (e.g. bacterial DHFR enzyme 1000x more sensitive to aminoglycosides than mammalian)
- Reliance on target (sulphonamide)
- Absence from host (β-lactams)

52
Q

What are some virulence factors H.Pylori utilises?

A
  • Very motile (multiple flagella)
  • Has BabA/B adhesins which bind epithelial cells
  • Neutralisation of stomach acid via urease production
  • Pore forming VacA forming anion selective channel (= water influx)
  • CagA injected interfering with signalling increasing cell proliferation (T4SS injector)
  • Induces IL-8 production (attracts PMNs)
53
Q

How can antibiotics AID the colonisation of C.diff resulting in pseudomembranous colitis?

A
  • Anaerobic spore-forming bacterium; colonises colon after antibiotics disrupt microflora
  • Secretes TcdA and TcdB toxins (glycosylate small GTPases) = subverted cytoskeleton and tight junction disruption (leaky epithelium/inflammation)
  • Treated using faecal transplants
54
Q

What broad mechanisms do bacteria use to resist antibiotics?

A

Antibiotics = huge evolutionary selection pressure for bacteria. Therefore resistance prized:

  • Enzyme mediated inactivation
  • Alteration to target
  • Metabolic bypass
  • Efflux pumps (multi drug resistance)
55
Q

Describe some examples of antibiotic resistance due to enzyme mediated inactivation:

A

β-lactamases cleaves penicillin (forming penicilloic acid):
- Stops penicillin mimicking D-Ala-D-Ala peptidoglycan crosslink
- Cannot bind to active site of transpeptidase
- Cannot stop cell wall synthesis (causing cell lysis)

Acetyl transferases prevent chloramphenicol binding ribosomes:
- Cannot binds 50S subunit - Does not inhibit peptidyl transferase (polypeptide elongation)

56
Q

Describe some examples of antibiotic resistance due to alteration to target:

A

Bacterial ribosome protection proteins (RPPs): - Stop tetracycline binding 30s subunit
- tRNAs can still bind

Onr binds topoisomerase blocking fluoroquinolones binding:
- Nucleic acid synthesis can continue

Synthesis of D-Ala-D-Lac alternative to D-Ala-D-Ala:
- Vancomycin can no longer bind to block transpeptidase action

57
Q

Describe example of antibiotic resistance due to metabolic bypass:

A

Alternative folate for amino acid synthesis
- Use different enzymes with much lower affinity for antibiotic (E.g. DHFR replaced by trimethoprim)

58
Q

Describe some examples of antibiotic resistance due to efflux pumps:

A
  • Ejection of drugs (bind to inner membrane transporter)
  • Ejected through ToIC exit duct system (spans periplasm)
  • Two component transporters: transporter (inner membrane) + porins on outer membrane
  • Could be a new potential target!
59
Q

How may a chronic bacterial infection occur?

A
  • Treatment/immunity eliminates sensitive population but persister cells remain (resuscitate)
  • Can occur stochastically (randomly)
  • Or induced by stresses (metabolic stress or antibiotics) – resistant bacteria multiply
  • Differences in a bacterial population (quorum sensing involved)
60
Q

What are some examples of a chronic bacterial infection?

A

Intracellular (M.TB; Chlamydia; Brucella; Salmonella)
- Infect macrophages
- Salmonella in bone marrow
- Brucella and salmonella in reticuloendothelial system

Extracellular (H.Pylori)

61
Q

How is a granuloma organised to contain infection?

A
  • Phagocytes (T, B, DC and neutrophils) surround infected macrophages
  • Activated macrophages can fuse to form giant cells
  • May have caseous necrosis in centre
  • T/B cells subsequently recruited
  • Lesion sealed off by epithelioid cells (can become calcified or fibrotic) = wound healing response

Allows local pro-inflammation (+ve feedback of TNF-α and cytokines) with systemic down-regulation of inflammation (Tregs; IL-10; TGF-β)

62
Q

How do bacteria respond to granuloma formation to remain viable?

A

Reduced metabolism:
- Slow replication

Manipulate phagosome:
- Prevent maturation into endo-lysosomal fusion
- Shown by IgG labelled latex beads – follow endosome pathways

Factor expression to manipulate endosome:
- Isocitrate lyase (ICL) = metabolism of fatty acids
- PE/PCRS outer membrane proteins = antigenic variation
- MprA = transcriptional regulation of persistence genes

63
Q

How does the host immune system antagonise a granuloma?

A
  • T cells and macrophages upregulated by IFNα and IFNγ = phagosomal fusion and acidification

Phagocyte activation:
- RNI and ROS
- Antimicrobial peptides
- Immune regulators (LRG-47 = immunity related GTPase)
- Proinflammatory cytokines (TNF-α, IL-18, IL-23)

Biology of Disease (7 decks)

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