microbiology Flashcards

1
Q

Which five agents cause infection?

A
  • viruses
  • bacteria
  • fungi
  • parasites
  • prions (mis-folded proteins)
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2
Q

Which three factors allow an infection to occur?

A
  • barriers to infection
  • environment
  • growth factors
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3
Q

What are viruses?

A
  • small, metabolically inert structures which need living host cells to replicate inside
  • infect animals, plants and bacteria
  • different shapes
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4
Q

What are the three major components of a virus?

A
  • genetic material (DNA/RNA)
  • protein coat (capsid)
  • lipid envelope derived from the host cell (some viruses)
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5
Q

Describe a T4 bacteriophage.

A
  • genetic material but no organelles (rely on host’s organelles to reproduce)
  • use surface protein(s) to bind to cell + insert genetic material into it
  • formation of biologicalvirusesduring the infection process in target host cells
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6
Q

What are bacteria?

A
  • unicellular, cell membrane, cell wall
  • genetic material is free DNA (asexually reproduce)
  • some move using flagella and attach via fimbriae
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7
Q

How can bacteria be classified?

A
  • shape → coccus, spirillum, bacillus
  • ability of cell wall to take up stain; G+VE/G-VE (determines structural strength → survival in environment)
  • name → Genus species (italics/underlined)
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8
Q

What are the four stages of gram-staining and the results that we should receive for a Gm+VE and Gm+VE cell?

A

• Stage 1: primary dye

  • reagent: crystal violet
  • colour (G+VE): purple
  • colour (G-VE): purple

• Stage 2: trapping agent

  • reagent: iodine
  • colour (G+VE): purple
  • colour (G-VE): purple

• Stage 3: decolouriser

  • reagent: alcohol/acetone
  • colour (G+VE): purple
  • colour (G-VE): colourless

• Stage 4: counter-stain

  • reagent: safranin/carbol fuchsin
  • colour (G+VE): purple → thick peptidoglycan cell wall retains primary stain
  • colour (G-VE): pink → thin peptidoglycan cell wall does not retain primary stain and is protected by lipophilic outer cell membrane
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9
Q

Describe fungi.

A
  • own eukaryotic kingdom → cell membrane, cell wall, nucleus and cytoplasmic structures
  • reproduce sexually + asexually
  • can be yeasts (Candida albicans) or molds (Aspergillus fumigatus) or diamorphic (switch between both forms)
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10
Q

What are the three types of parasite? Give an example of each.

A
  • ectoparasites → live outside host body i.e. fleas, ticks (type of spider)
  • endoparasites → live inside host body i.e. worms
  • epiparasites → parasite which lives on another related parasite i.e. malaria
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11
Q

What are the two general classes of human parasite?

A
  • unicellular organisms (protozoa)

- parasitic worms (helminths)

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12
Q

What type of life cycles do parasites have and what are many human infections classed as?

A
  • often complex life cycles which involves other animal(s)

- “accidental”

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13
Q

Describe prions.

A
  • smallest infective agent → proteinaceous infectious particles which lack nucleic acid (non-living)
  • proteins fold abnormally and accumulate, mainly in neural tissue → very difficult to destroy
  • concerns over cleaning surgical instruments
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14
Q

How do different viruses infect host cells for different lengths of time and what does this mean?

A
  • some stay dormant in host with symptoms re-appearing months/years later
  • others immediately leave host cells and symptoms rapidly appear
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15
Q

Give examples of viruses.

Hint - liver one with the alphabet

A
  • chickenpox virus/varicella → can lay dormant for decades, emerging to cause shingles
  • rhinovirus → infects hosts for days, causing a cold
  • hepatitis C → chronic liver infection over years
  • severe → ebola, SARS coronavirus (severe acute respiratory syndrome)
  • variable → flu (different viral influenza strains)
  • mild → rhinovirus (causes the common cold), herpes simplex (STI that causes cold sore/genital sores)
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16
Q

Give examples of bacterial diseases.

Hint - ‘m’ for blood, ‘b’ for heart, ‘c’ for skin and ‘s’ for throat

A
  • meningococcal sepsis → bacteria enter blood and multiply, damaging walls of blood vessels causing bleeding into skin and organs
  • bacterial endocarditis → infection of inner lining of heart
  • cellulitis → common, serious bacterial skin infection
  • streptococcal throat infection → at the back of the throat
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17
Q

Give examples of mild and severe fungal infections in immunocompromised patients.

(Hint - mild → TAR - THG person, talcum powder and the circles on potatoes, severe → IC)

A
• mild 
- thrush
- athletes foot
- ringworm
• severe (in immunocompromised):
- cryptococcal meningitis → HIV patients
- invasive candida (infection caused by yeast) → ICU
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18
Q

What is parasitic disease giardia?

A
  • bloody diarrhoea, caught from drinking infected water, may be seen in stool under a LM
  • cyst formed aids survival + spread
  • reproduces by binary/multiple fission or sexually (or both)
  • individual protozoon is hermaphroditic (an organism which produces gametes normally associated with M and F sexes)
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19
Q

What is the parasitic disease malaria?

A
  • one of the biggest killers worldwide
  • complex life cycle
  • reproduces in female anopheles’ mosquito and infects human RBCs
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20
Q

What are the four types of malarial parasite and which problem has arisen from different strains in different areas?

(Hint - P. FVOM)

A
  1. Plasmodium falciparum (most common)
  2. P. vivax
  3. P. ovale
  4. P. malariae
    - different types occur in different geographical areas w/ some overlap; resistance to treatment now problem
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21
Q

What are the different types of helminths (parasitic worms)?

(Hint - C(T), T(F), N(R) and last example rhymes with colitis and made of elephants)

A

• cestodes (tapeworms) → segmented, flat - fish, pork, beef tapeworms: can cause malabsorption or in variety of chronic diseases
• trematodes (flukes) → unsegmented, flat, oval worms
- lung flukes, liver flukes, pancreatic flukes, intestinal flukes, blood flukes (i.e. schistosoma)
• nematode (round worm) → biggest family which is cylindrical, with digestive tract, lips, teeth and anus
- (diarrhoea/malabsorption) e.g. elephantiasis caused by filarial worms asymptomatic or syndrome elephantiasis (severe swelling of limbs)

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22
Q

What is the helminth (blood fluke) schistosoma, how does it travel and what are its symptoms?

A
  • clinical disease commonly found in children who play in water → socioeconomically devastating
  • goes from: fresh water snails → flukes penetrate skin → adult worms migrate to veins → worms live + lay eggs for rest of host’s life → eggs penetrate vascular endothelium, enter bladder/gut + excreted in urine/stool to freshwater
  • symptoms → diarrhoea, fever, abdominal pain, hepatosplenomegaly/cystitis, urethritis, eventually bladder cancer
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23
Q

What are examples of diseases caused by prions (misfolded proteins)?

(a CV is BS …K? where only 1 + 2 haven’t gone paagal and ‘S’ for in sheep)

A
  1. CJD (Creutzfeldt-Jakob disease) – fatal, degenerative neurological disease - transmitted via contaminated hGH, surgical instruments and corneal grafts
  2. variant CJD - typically occurs in young adults
  3. BSE - another form of ‘mad cow disease’ that occurs in cattle
  4. scrapie – virus that occurs in sheep
  5. kuru- similar to vCJD (‘mad cow disease’) thought to be spread by cannibalism
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24
Q

Why do pathogens need nutrients and how can microbes inhabit so many possible environments?

A
  • to meet energy needs and provide necessary elements (CHON) to synthesise building blocks
  • successful in obtaining nutrients from variety of sources
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25
Q

Why does growth and reproduction of microbes require energy?

A
  • synthesis of new molecules, main building blocks (protein, DNA, RNA) and precursors (i.e. FAs, AAs, nucleic acids, carbohydrates)
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26
Q

Define metabolism.

A

all biochemical reactions that take place inside the cell to maintain its viability, growth and reproduction

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27
Q

What is a catabolic pathway and an anabolic pathway?

A
  • catabolic: break down molecules to produce energy (larger substrates, smaller products)
  • anabolic: use energy to combine small molecules into macromolecules (energy + source of elements - C)
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28
Q

What is the organism’s:

a) energy source if the name includes ‘photo?’
b) energy source if the name includes ‘chemo?’
c) carbon source if the name includes ‘auto?’
d) carbon source if the name includes ‘hetero?’
e) electron donor source if the name includes ‘organo?’
f) electron donor source if the name includes ‘lito?’

A

a) light
b) chemical compounds
c) CO₂
d) organic compounds
e) organic compounds
f) inorganic molecules

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29
Q

If an organism lacks ability to produce essential compound in body then how must it be obtained?

A

consumed in diet

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30
Q

What are E. Coli mostly composed of and which compounds act as catalysts in synthesis processes?

A
  • water

- other compounds e.g. vitamins

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31
Q

What is passive diffusion compared to active transport?

A
  • passive diffusion: no energy needed, driven by conc. gradient.
  • active transport: requires energy, requires receptors and work even against conc. gradient
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32
Q

What is group translocation?

A

less energy, involved phosphorylation of molecule

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33
Q

What are the physical requirements of microbial growth?

Hint - TOWPLP

A
• temperature → affects protein structure + fluidity of cytoplasm and cytoplasmic membrane, requirements can differ (i.e. thermophiles)
• water → all bacteria require ‘wet’ habitat as drying kills them
- pH
- osmolarity
• oxygen
• pressure
• light
• physical space availability
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34
Q

What is optimum growth temperature?

A

temp at which metabolic activity is at its peak and thus growth rate highest

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35
Q

What is ‘water activity’ (Aw) and how does it affect bacterial growth?

A

• vapour pressureof a sample divided by that of pure water at sametemp

  • low Aw → high solutes conc. (hypertonic solution)
  • bacterial growth correlates to Aw more accurately than absolute water content
  • usually required at least 0.8
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36
Q

How does pH affect microbe growth?

A
  • high/low pH inhibit microbial growth
  • acidic conditions of some body parts are defence mechanism (e.g. stomach and vagina)
  • acidophiles can tolerate acidic conditions and alkalinophile lives in alkaline media (i.e. soil and alkaline water like Vibrio cholera)
  • interacellular pH usually near normal
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37
Q

What is an:

a) obligate aerobe? (Hint – oxygen is obligatory)
b) anaerobe? (Hint – an-aerobes)
c) facultative anaerobes? (Hint – facultative means optional)
d) microaerophiles? (Hint – micro means a very small amount of tolerance)
e) aerotolerant microbe? (Hint – aerotolerant can survive without oxygen and can tolerate it too using enzymes)

A

a) requires O₂ for energy-production (respiration)
b) do not use O₂ for energy-production
c) can survive with or without O₂
d) can tolerate oxygen levels from 2-10% (limited ability to detoxify hydrogen peroxide and superoxide radicals)
e) anaerobes but have some enzymes that detoxify oxygen’s poisonous forms

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38
Q

What are the defence mechanisms of the body?

Hint - SMS-BIC

A
  • skin
  • mucus membranes
  • stomach acid
  • commensal microflora
  • immune system → innate or learnt
  • behaviour (e.g. good hygiene practices)
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39
Q

What are a pili and a flagellum found in bacterial cells?

A
  • pili - protein tubes extending out from outer membrane

- flagellum - whip-like structure outside cell wall responsible for movement

40
Q

Compare the following in bacterial cells and mammalian cells:

a) cell wall
b) nuclear membrane
c) ribosome subunits

A

a)
- bacterial cells: cell wall
- mammalian cells: no cell wall
b)
- bacterial cells: no nuclear membrane
- mammalian cells: nuclear membrane
c)
- bacterial cells: 30s and 50s
- mammalian cells: 40s and 60s

41
Q

In which three ways can bacteria be classified?

Hint - in the last category is chlamydia, rickets and mycoproteins

A

1) gram-stained bacteria
- gram +VE → aerobes/anaerobes
- gram –VE → aerobes/anaerobes
2) acid-fast bacilli (mycobacteria)
3) atypicals i.e. Chlamydiae, Rickettsiae and Mycoplasmas not classed as bacteria

42
Q

What is a pathogenic microorganism?

A
  • any microorganism capable of injuring its host

- e.g. by competing for metabolic resources, destroying its cells/tissues or secreting toxins

43
Q

State some injurious microorganisms.

A
  • bacteria
  • mycobacteria
  • viruses
  • fungi
  • protozoa
  • some helminths
44
Q

What are the portals of entry into the body for micro-organisms?

A
  • skin
  • respiratory tract
  • gastro-intestinal tract
  • urogenital system
  • conjunctiva
45
Q

State the six main natural immunity mechanisms

Hint - PIPATA

A
  • physical/chemical barriers
  • inflammation
  • phagocytosis
  • the complement system
  • antibacterial substances
  • antiviral substances e.g. IFNs
46
Q

What are the two forms of:

a) active immunity? Explain and provide examples.
b) passive immunity? Explain and provide examples.

A

a)
- naturally-acquired active immunity i.e. suffer from the infection
- artificially-acquired active immunity e.g. live vaccination
b)
- natural passive immunity e.g. mother passing antibodies to baby during pregnancy and breastfeeding
- artificial passive immunity e.g. antibodies injected from a serum (tetanus immunoglobulin)

47
Q

What is an antibiotic and what are the two types?

A
  • substance produced by micro-organisms/synthetically produced that selectively destroys or inhibits growth of other micro-organisms
    • either:
  • bactericidal (– kill bacteria)
  • bacteriostatic (– suppress growth/reproduction of bacteria)
48
Q

What are the different areas/processes in a bacterial cell that antibiotics can use to stop bacteria from working?

(HInt - CCDDRPP)

A
  • cell wall synthesis
  • cell wall integrity
  • DNA synthesis
  • DNA gyrase
  • RNA polymerase
  • protein synthesis - 50S/30S inhibitors
  • phospholipid membranes

(see notes)

49
Q

For each mechanism of action in bacterial cells, state antibiotic class/antibiotics and the basis for selective toxicity:

a) inhibit bacterial cell wall synthesis
b) inhibit bacterial protein synthesis
c) inhibit folate synthesis
d) inhibit transcription of bacterial RNA
e) inhibit DNA gyrase & topoisomerase

A

a)
- antibiotic/s: beta-lactamase, glycopeptides
- basis: beta-lactams are structural analogues (identical structure) of cell wall precursors → inhibit enzymes involved in cell wall synthesis
b)
- antibiotic/s: aminoglycosides, chloramphenicol, sodium fusidate, macrolides, tetracyclines
- basis: bacterial ribosomes have different RNA content and protein composition
c)
- antibiotic/s: sulphonamides, trimethoprim
- basis: inhibit dihydrofolate reductase (enzyme) which helps build DNA and synthesises folic acid
d)
- antibiotic/s: rifampicin
- basis: binds to bacterial DNA–dependent RNA polymerase
e)
- antibiotic/s: quinolones
- basis : modulate (controls) replication/expression of DNA

50
Q

How do beta-lactam antibiotics act on cell walls?

A
  • interfere with cross-linkage of peptidoglycans → bactericidal
  • i.e. penicillins and cephalosporins
51
Q

How do glycopeptide antibiotics act on cell walls?

Hint - don’t break inhibit the formation of…

A
  • inhibit peptidoglycan formation → bactericidal

- e.g. vancomycin, teicoplanin

52
Q

Describe the activity of penicillins.

Hint - PBPs similar to what and affect not just the cell wall

A
  • bacteria contain up to 8 penicillin-binding proteins (PBPs)
  • PBPs structurally similar to D-alanine-D-alanine residue of peptidoglycan so their function can be modified
  • weaken cell wall and act on biosynthesis, cell division, shape formation → bactericidal
  • spectrum of penicillin activity dependent on nature of groups attached to β-lactam ring
53
Q

Name antibiotics with β-lactam rings in their structure.

Hint - one you’re allergic to, 3 Cs and then ‘one’ bacteria

A
  • penicillins
  • cephalosporins
  • carbapenems
  • clavams
  • monobactams

(see notes for diagrams)

54
Q

State the mode of action of vancomycin using the diagrams.

A
  • N-acetylglucosamine (G)
  • N-acetylmuramic acid (M)
  • G and M attach to phospholipid carriers, allowing joining of them as dimers (-G—M—G—M—G- etc…)
  • dimers tacked onto existing peptidoglycan and phospholipid carrier released
  • vancomycin binds glycopeptides to prevent this release, hence further peptidoglycan formation
  • kills the G+VE cell

(see notes for diagrams)

55
Q

What is daptomycin (i.e. lipopeptide) as an antibiotic which can act on cytoplasmic membranes?

(Hint - from what, does what to cell, type of antibiotic, bac. cells it affects, how well it penetrates lungs)

A
  • from Streptomyces roseosporus
  • depolarisation of cell membrane
  • bactericidal to G +ve organisms including MRSA and VRE → poor lung penetration
56
Q

Which side-effects can lipopeptides have?

Hint - two types of ‘-pathy’

A
  • peripheral neuropathy (neuronal disorder)

- myopathy (muscular problems)

57
Q

What are polymixins (colisin) as antibiotics which can act on cytoplasmic membranes?

(Hint - an affinity for which atypical bacterial cell and which type of antibiotic)

A
  • affinity for membrane in G-ve bacilli

- bactericidal

58
Q

Which four antibiotics interfere with protein synthesis and how? State whether they are bacteriostatic/bactericidal.

(Hint - TACL)

A
  1. tetracyclines - bind to 30s ribosomal subunit → bacteriostatic
  2. aminoglycosides - mRNA-ribosome attachment → bactericidal
  3. chloramphenicol (i.e. macrolides, lincosamides) - bind to 50s ribosomal subunit → bacteriostatic
  4. linezolid → bacteriostatic
59
Q

Name some of the antibiotics that interfere with nucleic acid synthesis and state how they work.

(Hint - Quinn and Topi and Dee, Rami with DeRvla, Metrona broke the thread)

A
  • quinolones (i.e. ciprofloxacin) - selectively inhibits DNA gyrase + topoisomerase IV needed to separate bacterial DNA → inhibit cell division
  • rifampicin - inhibits DNA-dependent RNA polymerase activity by forming stable complex with enzyme → suppresses initiation of RNA synthesis
  • metronidazole - binds to bacterial DNA → strand breakage
60
Q

Which two antibiotics interfere with a metabolic pathway and how do they work?

(Hint - trimester and sulfon)

A

• trimethoprim -
- inhibits dihydrofolate reductase in bacteria:
reduction: dihydrofolate → tetrahydrofolate (active folic acid form)
• sulphonamides - work earlier in process

61
Q

Which three huge advances in medicine have antibiotics enabled?

A
  • now nearly zero deaths from sepsis after childbirth
  • organ transplantation
  • chemotherapy treatment
62
Q

When are antibiotics used?

A
  • 50% use in humans and animals each

- mostly primary care (GP, community and dental) → prescribing declined but still inappropriate prescriptions given

63
Q

What is the problem surrounding antibiotic use?

A

• more use of antibiotics = more resistant bacteria

  • use selects for resistant bacteria
  • resistance increases clinical complications, hospital stay and death
  • developing new antibiotics is expensive + slow
  • antibiotics increasingly losing effectiveness
  • i.e. Methicillin resistant Staphylcoccus aureus (MRSA)
64
Q

How can we reduce antimicrobial resistance (AMR) and preserve the utility of available drugs for as long as possible?

A

reducing antimicrobial selection pressure

65
Q

What are the two types of antibiotic resistance?

Hint - IN

A
  • natural resistance

- intrinsic resistance

66
Q

For which three reasons can an entire species become resistant before any antibiotic is introduced?

(Hint - can’t get through, no place to land, cell’s ABs kill it before it can land)

A
  • lack of penetration through cell wall
  • lack of suitable cell wall target site
  • susceptibility of antibiotic to naturally-produced enzymes
67
Q

What is the main strategy that can be used to reduce antimicrobial resistance (AMR)?

A
  • decrease antibiotic use as it encourages resistance (even normal bacteria flora receiving antibiotic)
68
Q

Which mechanisms have bacteria evolved to evade antimicrobial drugs?

(Hint - CA with sister ‘tids)

A
  • chromosomal mutations

- acquisition of resistance genes → via conjugation, transduction and transformation

69
Q

Define:

a) conjugation (Hint - to conjugate is to move from one part to another)
b) transduction (Hint - to carry something from one place to another)
c) transformation (Hint - soak up something)

A

a) plasmids move from one bacteria to another
b) bacteriophages/phages move between bacteria sometimes carry genes
c) take up DNA from solution

70
Q

What can the mechanisms by which DNA is taken up also enhance?

(Hint - more problems)

A

the possibility of multi-drug resistance

71
Q

What are the possible mechanisms of resistance for bacteria against antibiotics?

(Hint - the DIAMA)

A
  • DNA transfer between different bacteria species
  • inactivation of antibiotic by bacterial enzymes produced i.e. lactamases and aminoglycoside-modifying enzymes
  • alteration of antibiotic at the target site
  • modification of bacteria well wall protein
  • activation of drug efflux pump

(although most organisms have resistance mechanisms causing inactivation of drug, single organism may carry a mix of resistance capabilities)

72
Q

For each antibiotic, state the:

  • target
  • mechanism
  • bacteria affected
    a) beta-lactamse
    b) glycopeptides
    c) macrolides
    d) tetracyclines
    e) quinolones
    f) rifampicin
    g) sodium fusidate
    h) trimethoprim
A

a)
- target: PBPs
- mechanism: alterations to structure of PBP so reduced affinity for beta-lactams
- bacteria affected: Staph. aureus, Strep.pneumoniae, Neisseria gonorrhoeae
b)
- target: peptidglycan precursors
- mechanism: substitution of D-alanine-D-alanine binding site w/ D-alanine-D-lactate
- bacteria affected:
c)
- target: ribosome
- mechanism(s):
• production of enzymes that methylate specific adenine residues on ribosomal RNA
• mutations affecting structure of ribosomal protein L4 /nucleotide sequence of specific regions of ribosomal RNA
- bacteria affected:
• Streptococcus sp.
• Strep. pneumoniae
d)
- target: ribosome
- mechanism: production of ribosomal protection proteins that cause release of bound tetracycline
- bacteria affected: wide range of gram +ve and -ve species
e)
- target: DNA gyrase and topoisomerase
- mechanism: DNA gyrase and topoisomerase
AA changes in specific regions of enzymes resulting in reduced affinity for quinolones
- bacteria affected: wide range of gram +ve and -ve species
f)
- target: DNA-dependent RNA polymerase
- mechanism: AA changes in the B-subunit reduce its affinity
- bacteria affected: wide range of gram +ve and -ve species
g)
- target: elongation factor G
- mechanism: alteration of structure
- bacteria affected: Staph. aureus
h)
- target: dihydrofolate reductase
- mechanism: production of new trimethoprim-insensitive enzyme in addition to normal enzyme
- bacteria affected: Enterobacteriaceae

73
Q

Which huge problem has been created due to antibiotic resistance? Name the main ones.

(Hint - CCEMM)

A

“superbugs”

  • CDAD: C.difficile associated diarrhoea
  • CPE: Carbapenemase-producing Enterobacteriaceae
  • ESBL: Extended-spectrum beta-lactamases (resistance → more difficult to treat)
  • MERS: Middle East respiratory syndrome coronavirus (MERS-CoV) - viral respiratory disease with symptoms → fever and cough progress to severe pneumonia + SOB
  • MRSA: meticillin-resistant Staphylococcus aureus (G+VE bacterium that causes skin infections and systemic infections including bacteraemia, endocarditis, bone and joint/respiratory tract infections)
74
Q

What is MRSA resistant to?

A

methicillin and antibiotics commonly-used to treat S. aureus infections

75
Q

What are the five main strategies to reduce AMR?

A
  1. prevention of infection e.g. better sanitation, hand hygiene, vaccines
  2. better diagnostics → identifying bacterial Vs viral infections
  3. reduce antibiotic use/ minimise antibiotic use
  4. development of new classes of antibiotics e.g. research support, orphan drug status/fast-track
  5. public health awareness through campaigns and antibiotic guardian
76
Q

What is a HAI (hospital-acquired infection)?

A

an infection caught while hospitalised (medically known as nosocomical infections)

77
Q

What are the four most common types of HAI?

Hint - lungs, scalpel, catheter and blood

A
  • respiratory infections (including pneumonia and infections of lower RT)
  • urinary tract infections (UTIs)
  • surgical site infections (SSIs)
  • sepsis (increasing)
78
Q

What are the risk factors for nosocomial infection?

Hint - I’M HAUTI

A
  • hospital stay duration
  • indwelling (internal) catheters
  • mechanical ventilation
  • total parenteral nutrition (IV feeding/nutrition)
  • antibiotic usage
  • use of histamine (H2) receptor blockers (induces bacterial overgrowth) which reduce acid production in stomach
  • age — more common in neonates, infants and the elderly
  • immune deficiency
79
Q

Which bacteria do HAI surveillance programmes cover?

A
  • bacteraemia
  • gram-VE bacteria
  • Clostridioides difficile infection
  • Escherichia coli
  • Pseudomonas aeruginosa
  • Klebsiella species
  • Staphylococcus aureus ([methicillin-resistant Staphylococcus aureus], MRSA and [meticillin sensitive Staphylococcus aureus] MSSA)
  • Surgical site infection
80
Q

What are ESBLs?

A

bacteria-produced enzymes resistant to cephalosporins (their antibiotics)

81
Q

What is the significance of ESBLs in antibiotics?

A
  • new class of ESBL (CTX-M enzymes) emerged widely-detected among E. coli
  • ESBL-producing E. coli can resist penicillins and usually (1st-3rd generation) cephalosporins
  • ESBLs most often found in UTIs
  • plasmids also contain resistance genes to ciprofloxacin and trimethoprim
  • there are also AmpC beta-lactamases resistant to antibiotics
82
Q

What are the treatment options for ESBLs and AmpC?

Hint - an ACCouNTanTT

A
  • aminoglycoside
  • carbapenem
  • ciprofloxacin
  • trimethoprim
  • nitrofurantoin
  • tigecycline
  • temocillin
83
Q

What is hospital-acquired or nosocomial pneumonia (HAP)?

A
  • anypneumoniacontracted by a patient inthe hospitalat least 48–72 hours after admission
    → different to community-acquired pneumonia
84
Q

What is a UTI and what is it caused by?

A
  • infection involving any part of urinary system (urethra, bladder, ureters and kidney)
    → most common HCAI
  • UTI bacteria
  • 75% associated with urinary catheter
  • most important risk factor for developing catheter-associated UTI (CAUTI) is prolonged use
85
Q

Which bacteria cause a UTI?

A

enteric pathogens (e.g.E. coli) most commonly responsible but also:

  • Pseudomonasspecies
  • Enterococcusspecies
  • Staphylococcus aureus
  • Coagulase-negative staphylococci
  • Enterobacterspecies, and yeast also known to cause infection
  • Proteusand Pseudomonasspecies are organisms most-commonly associated w/ biofilm growth on catheters
  • Candida, especiallyCandida albicans, is 2nd-most-common organism that causes CAUTI
86
Q

What is E. coli and where it can be found?

A
  • E. Coli Bacterium → Gm-VE, facultatively-anaerobic, rod-shaped, coliform (genus Escherichia)
  • commonly found in lower intestine of warm-blooded organisms
87
Q

What is sepsis and its signs/symptoms?

A
- a life-threatening condition which arises when the body's response to infection causes injury to own tissues and organs
• symptoms: 
- fever
- increased HR
- increased breathing rate
- confusion
88
Q

When are you more likely to devleop sepsis?

A
  • recently had surgery
  • urinary catheterfitted
  • in hospital for long time
89
Q

For each body area, which other condition is a UTI usually associated with:

a) GI tract?
b) GU (genitourinary) tract?
c) pelvis?
d) lower respiratory tract?
e) vascular system?
f) heart and cardiac vasculature?

A

a) liver, gallbladder or colon disease, abscesses, intestinal obstruction and GI instrumentation
b) pyelonephritis, intra- or perinephric abscess, renal calculi, urinary tract obstruction, acute prostatitis/abscess, renal insufficiency and GU instrumentation
c) peritonitis and pelvic abscess
d) community-acquired pneumonia (+ asplenia), empyema and lung abscess
e) infected IV line/prosthetic device
f) acute bacterial endocarditis and myocardial/perivalvular ring abscess

90
Q

What is MRSA and how resistant is it?

A
  • a gram-positive bacterium genetically-different from other strains of SA
  • often resistant to several antibiotic treatment types
  • mostS. aureusmethicillin-susceptible but not MRSA - now resistant to all forms of penicillin and cephalosporin
  • different toM SSA (Methicillin-sensitive SA)
  • 1 in 3 people carry staph in the nose, usually without any illness
91
Q

Using the diagram in the notes, what are the four stages of the transpeptidation of the mechanism of action for penicillin?

A
  • peptidoglycan made up of chains of N-acetyl glucosamine (G) and N-acetylmuramic acid (M), with tetrapeptide chains attached to each M, cross-linked with glycine bridges
  • penicillin mechanism of action:
    1. penicillins attach to PBPs
    2. disrupts cross-linking of chains
    3. weakens structure
    4. lysing of (MRSA) bacterial cell
92
Q

What is the MRSA bypass mechanism?

A
  • some MRSA variants modified PBP’s so penicillins can’t bind (organisms resistant to beta-lactams)
  • beta-lactam ring (binding area) modified, hence with a new ring antibiotics ineffective
93
Q

What is C. diff, where in humans does it inhabit and how is it transmitted?

A
  • spore-forming, anaerobic, Gram +VE, bacillus bacterium
  • spores → facilitate organism survival in adverse conditions (heat, drying, stomach acids etc…)
  • produces exotoxins (bacterial toxin) A and B
  • human habitat: large intestine (v. little O₂) and found in soil
  • faeco-oral transmission
94
Q

What is CDAD and its different forms?

A
- when C. diff Associated Diarrhoea (CDAD) toxins inflame intestinal wall resulting in disease:
• antibiotic associated diarrhoea (AAD)
• antibiotic associated colitis (AAC)
• pseudomembranous colitis (PMC)
• fulminant colitis (very severe)
95
Q

What is colitis?

A

inflammation of inner lining of colon

96
Q

How is the extent of CDAD severity assessed and why must it be very quickly diagnosed and treated?

A
  • sigmoidoscopy (test to examine lining of sigmoid colon using endoscope) + biopsy or non-invasive methods, i.e. CT
  • the patient can very quickly progress through its four stages