bacterial infections 1 adrian Flashcards

1
Q

how do pathogenic bacteria survive?

A

– must remain in close contact with the body and multiply – must survive host defence – must compete against endogenous flor

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2
Q

what do symptoms of infection arise from?

A

the direct effect of the bacteria eg diarrhoea with salmonela
- the host immune response

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3
Q

how does the host prevent bacteria multiplication?

A

– bacteria multiplies uncontrollably resulting in death of host
– host removes bacteria (possibly with the help of antibiotics)
– equilibrium reached where both live in balan

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4
Q

what are the different phases of growth?

A
  • Lag phase – very little to no reproduction – maturation – synthesis
  • Log phase – number of cells doubles at constant exponential rate
  • Stationary phase – population of rate of cell death equals cell growth
  • Death phase – population of rate of cell death greater than cell growth
  • Dormant – Lack of nutrients for growth
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5
Q

what does selective toxicity require?

A
  • Selective toxicity to microorganism
  • Limited / low toxicity to the human or mammalian host
  • Relies upon differences between microbial and mammalian cells – structure – function – biochemistry
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6
Q

what are the difference between pro and eukaryotic cells?

A
  • Bacterial cell has a cell wall and plasma membrane the cell wall protects the bacteria from differences in osmotic pressure
    and prevents swelling and bursting due to the flow of water into the cell – extra specific targets that mammalian host does not have
  • Bacterial cells do not have defined nuclei – easy access to DNA as target
  • Bacterial cells are relatively simple and do not contain organelles
    e.g. mitochondria
    – easy access to metabolic processes as targets
    the biochem is v different to eukaryotic cells eg vitamin synthesis
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7
Q

what is gram +ve and -ve cell wall staiend with?

A

+ve= crystal violet-iodine xomplex
-ve= does not reatain gram stain

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8
Q

can you have gra +ve and -ve?

A
  • Some antibacterial agents are active against both Gram positive and Gram negative
    bacteria (note, generalisation and is drug/bacterial strain dependant)
    – b-lactams (broad spectrum G-ve and many G+ve
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9
Q

what is a simple structure of a gram +ve bacterial cell wall?

A
  • Simple structure – peptidoglycan
    outer layer
    – no outer membrane
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10
Q

what does peptidoglycan consist of?

A

parallel sugar backbones composed of
alternating NAG and NAM

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11
Q

what are attached to the NAM through the CA residue?

A

peptide chains
they are linked together to give extra strength to the cell wall through cross link formation, catalysed by peptidoglycan transpeptidase

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12
Q

what is the structure of gram -ve bacteria cell wall?

A
  • More complex structure
  • peptidoglycan linked to outer membrane
    (phospholipid/lipopolysaccharide)
  • Entry to cell via porins found in both
    outer and inner membranes
  • Effective barriers to hydrophilic compounds and large molecules
  • More selective uptake
  • Uptake of antibiotics effectively through internalisation via porins
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13
Q

what is the structure of a mycolic bacterial cell wall?

A
  • Abnormally thick, viscous and waxy mycolic acid outer layer
    – low expression and activity of porin
    proteins
    – low permeability of cell
    – provides intrinsic resistance to antibacterial agents
  • Similar peptidoglycan cell wall to G+ve/G-ve with additional sugar-based
    structure
    – Little intrinsic resistance to agents targeting this
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14
Q

what are examples of gram +ve bacteria?

A
  • Gram positive obligate aerobes – Mycobacterium, Chlamydiae
  • Gram positive facultative – Cornebacterium, Enterococcus, Staphylococcus, Streptococcus, Listeria
  • Gram positive obligate anaerobes – Clostridium
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15
Q

what are examples of gram -ve bacteria?

A
  • Gram negative obligate aerobes
    – Legionella, Moraxella, Pseudomonas
  • Gram negative microaerophilic (lower 02 than atmosphere) – Campylobacter, Helicobacter
  • Gram negative facultative – Enterobacteria (Serratia and Enterobacter), Escherichia, Haemophilus, Klebsiella, Neisseria, Proteus, Salmonella, Shigella, Vibrio
  • Gram negative obligate anaerobes – Bacteroids
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16
Q

define commensal bacteria

A

symbiotic bacteria that gain benefit (residence, food) and cause no harm in usual site

17
Q

define nosocomial bacteria?

A

hospital acquired bacteria

18
Q

what is intrinsic resistance ?

A

through already existing mechanisms transmitted through generations of bacteria

19
Q

what is acquired resistance?

A

resistance developed towards bactericidal agents by gene mutation [rare] or in-colony transfer of plasmids carrying resistance genes
[common])

20
Q

what are some important clinical pathogens? ESKAPE+

A

– Enterococcus faecium (G+ve)
– Staphylococcus aureus (G+ve)
– Klebsiella pneumonia (G-ve)
– Acinetobacter baumannii (G-ve)
– Pseudomonas aeruginosa (G-ve)
– Enterobacter species (G-ve)
– Clostridioides difficile (G+ve) (Clostridium diffi

21
Q

what kind of bacteria poses the greatest threat?

A

G-ve bacteria considered to present the most serious clinical threat in hospitals – greater spread of resistance, even between species – fewer antibacterial agents available due to acquired resistance

22
Q

define pan drug resistant microorganisms

A

– non-susceptibility to all agents in all antimicrobial categories – (i.e. no effective antibacterial availabe)

23
Q

define extensively drug resistant microorganisms

A

– options available are highly limited – non-susceptibility to at least one agent in all but two or fewer antimicrobial
categories – (i.e. bacterial isolates remain susceptible to only one or two categories)

24
Q

define multi-drug resistant microorganisms

A

– options available are limited – non-susceptibility to at least one agent in three or more antimicrobial
categories – (i.e. bacterial isolates remain susceptible to more than two categories, but
three or more categories have non-susceptibility)

25
Q

what are the different types of microbiological resistance?

A
  • Intrinsic resistance (vertical transmission)
    – protection from antibacterials by natural bacterial defences, such as biofilms (Ps. aeruginosa, mycobacteria)
    – all strains of such species are resistant
  • Acquired resistance (horizontal transmission) – 4 main mechanisms
    – all acquired from another strain or species
    – (acquired resistance can then be passed through generations)
    – not all strains have same acquired resistance – acquired resistance individual to each occurrence of each strain
26
Q

what is clinical resistance?

A

the failure to achieve an antimicrobial concentration which inhibits the growth of an organism

27
Q

how do you get acquired resistance?

A
  • Most commonly transmitted on plasmids
28
Q

what are the 4 different acquired resistance mechanisms

A
  1. Acquire gene encoding for enzyme that can destroy antibacterial agent – e.g. b-lactamases destroy b-lactam antibiotics
  2. Acquire efflux pumps: siphon antibacterial out of cell – e.g. Quinolone resistance often due to acquired efflux pump genes
  3. Acquire several genes for biochemical pathway to alter cell wall: no binding site for antibacterial agent – e.g. vancomycin resistance
  4. Acquire mutations to porin gene: down-regulated expression leads to reduced access into bacterial cell – e.g. Loss of Omp K35 in E. coli and K. pneumoniae linked to cefoxitin
    resistance
29
Q

what does TARGET stand for?

A

– Treat Antibiotics Responsibly, Guidance, Education, Tools