bacterial infections 1 adrian Flashcards
how do pathogenic bacteria survive?
– must remain in close contact with the body and multiply – must survive host defence – must compete against endogenous flor
what do symptoms of infection arise from?
the direct effect of the bacteria eg diarrhoea with salmonela
- the host immune response
how does the host prevent bacteria multiplication?
– bacteria multiplies uncontrollably resulting in death of host
– host removes bacteria (possibly with the help of antibiotics)
– equilibrium reached where both live in balan
what are the different phases of growth?
- 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
what does selective toxicity require?
- Selective toxicity to microorganism
- Limited / low toxicity to the human or mammalian host
- Relies upon differences between microbial and mammalian cells – structure – function – biochemistry
what are the difference between pro and eukaryotic cells?
- 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
what is gram +ve and -ve cell wall staiend with?
+ve= crystal violet-iodine xomplex
-ve= does not reatain gram stain
can you have gra +ve and -ve?
- 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
what is a simple structure of a gram +ve bacterial cell wall?
- Simple structure – peptidoglycan
outer layer
– no outer membrane
what does peptidoglycan consist of?
parallel sugar backbones composed of
alternating NAG and NAM
what are attached to the NAM through the CA residue?
peptide chains
they are linked together to give extra strength to the cell wall through cross link formation, catalysed by peptidoglycan transpeptidase
what is the structure of gram -ve bacteria cell wall?
- 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
what is the structure of a mycolic bacterial cell wall?
- 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
what are examples of gram +ve bacteria?
- Gram positive obligate aerobes – Mycobacterium, Chlamydiae
- Gram positive facultative – Cornebacterium, Enterococcus, Staphylococcus, Streptococcus, Listeria
- Gram positive obligate anaerobes – Clostridium
what are examples of gram -ve bacteria?
- 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
define commensal bacteria
symbiotic bacteria that gain benefit (residence, food) and cause no harm in usual site
define nosocomial bacteria?
hospital acquired bacteria
what is intrinsic resistance ?
through already existing mechanisms transmitted through generations of bacteria
what is acquired resistance?
resistance developed towards bactericidal agents by gene mutation [rare] or in-colony transfer of plasmids carrying resistance genes
[common])
what are some important clinical pathogens? ESKAPE+
– 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
what kind of bacteria poses the greatest threat?
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
define pan drug resistant microorganisms
– non-susceptibility to all agents in all antimicrobial categories – (i.e. no effective antibacterial availabe)
define extensively drug resistant microorganisms
– 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)
define multi-drug resistant microorganisms
– 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)
what are the different types of microbiological resistance?
- 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
what is clinical resistance?
the failure to achieve an antimicrobial concentration which inhibits the growth of an organism
how do you get acquired resistance?
- Most commonly transmitted on plasmids
what are the 4 different acquired resistance mechanisms
- Acquire gene encoding for enzyme that can destroy antibacterial agent – e.g. b-lactamases destroy b-lactam antibiotics
- Acquire efflux pumps: siphon antibacterial out of cell – e.g. Quinolone resistance often due to acquired efflux pump genes
- Acquire several genes for biochemical pathway to alter cell wall: no binding site for antibacterial agent – e.g. vancomycin resistance
- 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
what does TARGET stand for?
– Treat Antibiotics Responsibly, Guidance, Education, Tools
