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FLS > Bacteria > Flashcards

Bacteria Flashcards

1
Q

Capsule

A

Extracellular Polysaccharide gel- high in water content
Protects bacteria from the immune system and stops them getting dehydrated

Only present in some species

May consist of a single sugar polymerised i.e glucose polymerised into glucan

Repeat units of two or more derivatives e.g glucosamine (amine of glucose) or glucuronic acid (CA of glucose)

Reducing oponisation (binding of antibodies) and phagocytosis

Closely surrounds the cell

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2
Q

Glycocalyx

A

Loose meshwork of fibrils extending outward from the cell
Plays a major role in bacterial adherence to surfaces
E.g Plaque - Streptococcus mutans

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3
Q

Cell wall

A

Divides bacteria into two groups: either positive or negative
Based on the retention of the crystal violet/iodine complex (G+ve) upon treatment with acetone/alcohol or its release from the cell
Positive: PURPLE (retention)
NEGATIVE: PINK
Coccus: ROUND
Bacillus: ROD

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4
Q

Cell wall composition

A

Gram +ve have a THICK layer of peptidoglycan which accounts for up to 90% of the dry weight of the wall

Gram -ve have a THIN layer of peptidoglycan but instead have periplasm either side (outer membrane, lipopolysaccharide and protein)

Peptidoglycan consists of a polymer of two sugars: N-acetylglucosamine
N-acetylmuramic acid (polymerised to form thin, long chains, target for most antibiotics)

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5
Q

Cell wall cross links

A

Gram +ve: Penta-glycine linkage

Gram -ve: Single bond linkage (D-ala to diamino-pimelic acid)

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6
Q

Envelopes

A

Gram -ve much more heavily modified:
Phospholipid bilayer
O-polysaccharde over activates your immune system
Lipidpolysaccharide (LPS) (O-specific polysaccharide, core polysaccharide, Lipid A) again elicits strong immune responses in animals

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7
Q

Immune response?

A

TLR (on surface of dendritic cell) senses the presence of LPS on the bacteria which leads to an immune response
could lead to overproduction, attack of bodies own cells

TLR4: detects flagellum

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8
Q

Fimbriae

A

Involved in adherence to surfaces

Genetic manipulation has shown that taking fimbrae away leads to NO disease

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9
Q

Type 1 Fimbriae

A

Expressed by many Gram -ve strands of bacteria
Binds to mast cells, T/B lymphocytes, neutrophils, macrophages
Mannose containing receptors for the FimH moiety: Neutrophils CD11/18 and CD66; macrophages and mast cells CD48.
Absence of Gal a(1-4) gal on inflammatory cells
Type 1 fimbriae are HIGHLY inflammatory
Attachment pilus

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10
Q

P-Fimbriae

A

Expressed by Pyelonephritis causing strains of E.coli (kidney infections)
Bind to Gal a (1-4) gal containing receptors
Receptor contains ceramide which is released upon binding
Activation of Thr/Ser kinases
Release of IL-8/IL-6
Functional mimic of normal TNF pathway

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11
Q

The pap gene cluster, to make P-fimbriae

A

10Kb of DNA coding for 11 proteins
These proteins are the structural proteins needed for the pilus itself and the machinery for assembly on the outer membrane

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12
Q

Flagella

A

Long, thin appendages
At one end polar
Many places around the cell ]
Helically shaped
Made of a protein called Flagellin
Passes through rings in cell wall (one for gram +ve, two for gram -ve)
Motor proteins drive flagellum and rotate filament
Fli proteins act as a switch to reverse the motor
Energy provided by the proton motive force (flow of protons through flagellum;drives rotation)
Important for chemotaxis (food)

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13
Q

Plasma membrane

A

Fluid mosaic

Integral membrane proteins: energy generation, transport into and metabolites out of the cell

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14
Q

Cytosol

A

Contains a complex mixture of proteins, ions, solute molecules as well as ribosomes
Allowing exchange within an environment

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15
Q

Endospores

A

e.g C.difficile
Spore is a resting cell, highly resistant to desiccation, heat and chemical agents
produced in response to environmental conditions e.g reduction in carbon and nitrogen sources, nutritional depletion
PRESERVES the organism

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16
Q

Nuclear area

A

Contains a single, long continuous circular double stranded DNA molecule = the bacterial chromosome
no histones

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17
Q

Plasmids

A

Extra chromosomal elements (5-100 genes)
Can be lost or gained without causing damage to cell
Antibiotic resistance

18
Q

Bacterial replication

A
  • Initiation, Elongation, Termination
  • Initiation oriC (fixed to cell membrane), DnaA (initiator protein oriC) DnaA ‘melts’ the DNA then DnaB is recruited (helicase); opens replication forks leaving OriC in both directions: BIDIRECTIONAL REPLICATION
  • Elongation: Primase (DnaG) lays down RNA primer and DNA polymerase III copies the DNA; Okazaki fragments, DNA ligase
  • Termination: Rep forks reach part of the chromosome opp oriC at ter sites: prevents DnaB activity (helicase) Completed chromosomes are linked and need to be resolved by topoisomerases to separate them. TWO SEPARATE daughter cells.
19
Q

polycistronic operons

A

Genes with similar functions in bacteria are ‘clumped’ together

20
Q

How do bacteria CONTROL their gene expression?

A

o Genetic change structure of DNA (make promotor bind harder/easier)
o Organisation Groups of genes controlled by one switch, produce them altogether
• Transcriptional regulators can turn genes on/off in response to environmental change (underpin bacterias ability to respond to stress; help/hinder binding of RNAP: BLOCKS promotor by binding to why RNAP would bind

21
Q

Regulon

A

TR protein may not only bind to one site, may be a whole load of genes that respond to the same stress: REGULONS

22
Q

How do bacteria evolve their DNA?

A

Simple mutations of Polymerase (mis-sense, non sense) SSP’s
Programmed mutations
Transfer of DNA: Transposition, Conjugation, Transduction, Transformation

23
Q

Transposition

A

Bits of DNA can move: transposons

Copy and Paste Class I transposition: RNA, reverse transcriptase and inserted elsewhere

Cut and paste Class II transposition cut out and inserted elsewhere by resolvase

Linked to AR

24
Q

Transduction

A

• Phage infects bacterial cell (virus that infects bacteria) passes genetic material from one bacterium to another
o Phage uses bacterial machinery to replicate itself; new viruses can sometimes assemble some bacterial DNA; lysed; passes on to new bacterium

25
Q

Transformation

A

• Uptake of NAKED DNA from environment incorporated into host genome

26
Q

Programmed mutations

A 
•	Programmed mutations: some genes are turned on/ off at high frequency (antigens) = PHASE VARIABLE 
o	PM  genes that end up on cell surface (involved in immune response) huge range of antigenetic profiles 
•	Phase variation: Genomic rearrangement, strand slippage, Methylation 
o	FimA (adhesion)  flip genes at high frequencies (on/off) promotor in wrong orientation; antigenetic profiles
27
Q

Sigma factor

A

A sigma factor (σ factor) is a protein needed only for initiation of RNA synthesis. It is a bacterial transcription initiation factor that enables specific binding of RNA polymerase to gene promoters.

28
Q

Antibacterial compound

A

• chemicals produced by microorganisms or plants (natural) or synthesised inhibits the growth of, and/or kills bacteria.
o Sometimes killing bacteria is worse releases toxins

29
Q

Anti-microbials

A

• Anti-virals, Anti-bacterials, Anti-fungals, Anti-malarials (kill or inhibit)

30
Q

Empiric screening

A

• Empiric screening Doctors testing any ‘soils’ they can get their hands on

31
Q

Some antibiotics in clinical use

A

B-lactams (e.g Penicillins) BIGGEST CLASS; Tetracyclines; Glycopeptides (Vancomycin); Macrolides (Erythromycin)

32
Q

4 Targets for antibacterial action

A

Cell wall synthesis inhibitor (B-lactams)
Cell membrane (Polymyxin)
Protein synthesis: Tetracyclines
Nucleic acid Synthesis: Sulphonamides

33
Q

Are antibiotics specific?

A
  • Cell wall: YES! Protein synthesis: most can discriminate P from E; Nucleic acid/cytoplasmic cell envelope: can act on P and E
  • Many drugs can inhibit enzymes in metabolic pathways which bacteria have to synthesise
  • Drugs can work at very low concentrations around bacteria but don’t work at these concentrations around humans
34
Q

Which antibiotic should I use?

A

• Clinical (e.g typical pathogen for that site, agents proven to be effective) Lab (isolation of pathogen, susceptibility of pathogen to different drugs)
o Where you’ve been… with whom?
• Determining susceptibility: Gradient concentration of drugs; MIC
o E-test numbers on stick tell you drug conc; colonies present are resistant strains
o Liquid culture (MIC) differing drug concentrations; sub-culture onto agar
o Concentration that kills can be different to MIC

35
Q

Downsides to antibiotics?

A

• Speed of action (Meningitis); Sensitivity of target (other bacteria? Host cells?); Adverse effects (side effects: trade off)

36
Q

Breakpoint concentration

A

Concentration BELOW which bacteria are classed as susceptible; different values in different countries (cultural decision)

37
Q

More than one antibiotic?

A

Concentration BELOW which bacteria are classed as susceptible; different values in different countries (cultural decision)

38
Q

Pharmacokinetics

A

• SERUM concentration over time in volunteers. Penetration to site of infection?

39
Q

Pharmacodynamics

A

Is the drug toxic? Does the drug kill at increasing concentrations or increasing exposure? PAE (post-antibiotic effect) wash A off does the drug still continue to work? Should we dose less often?
• Graphs If drug conc goes below MIC in 7 hours; new dose required

40
Q

Other issues to consider related to antibiotics?

A
  • What route? Topical; oral; intravenous; intramuscular stomach acid; properties of drug.. adverse reactions?
  • Less developed countries access to medicine unlikely to be taking correct medication/dose
  • Antibiotics also used in: Brewing, home(domestic use)
  • Antibacterials vs vaccines Mostly specific; higher toxicity; short duration of effect; duration of treatment may be prolonged; HIGH effectiveness
  • Providing evolutionary pressure for drug resistance to develop really close relationship between use and resistance
  • Mutations clonal spread of resistant genes; acquisition of foreign DNA: plasmids; mutation in/ or in recombination of genetic material
  • Bacteria and people MOVE around; no perception of what we are doing in a crowded environment

FLS (9 decks)

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