MICRO: Bacterial Infections Flashcards
1
Q
describe how bacteria use flagella and endospores
A
- flagella (made of flagellin protein): rotates like a propeller for motility
- endospores: 1 bacteria makes 1 heat resistant spore, allows it to persist in environment
2
Q
3 virulence factors which allow bacteria to adhere + examples of bacteria which use these
A
- pili + fimbriae (N. gonorrhoea): hair-like projections for adhesion to host + surfaces + other bacteria
- afimbrial adhesins (B. pertussis): surface proteins or ECM that allows it to adhere
- hydrated sticky polysaccharide capsule (e.g. S. pneumoniae): avoid phagocytosis, mimic human polysaccharides, adherence, mask surface antigens and binds factor H to prevent opsonisation
3
Q
actin mediated motility
A
- Listeria monocytogenes
- binds to cell plasma membrane and tricks it into inviting it into a vacuole, sometimes goes into bloodstream
- can also degrade vacuole: steals the cell’s actin to move into neighbouring cell, avoiding extracellular immune molecules
- picks up a double membrane and the process repeats
4
Q
how do biofilms form?
A
- capsules as well as fimbrial + afimbrial adhesins can allow bacteria to form biofilms
- difficult for immune system or antibiotics to penetrate and destroy
5
Q
which 3 enzymes do bacteria express that degrade host ECM?
A
- collagenase: breaks down collagen in ECM
- hyaluronidase: breaks down hyaluronic acid in ECM
- urease (H. pylori): cleaves urea to make ammonia which neutralises stomach acid so it can survive > causes stomach ulcers
6
Q
which 2 enzymes does S. aureus release which allows it to be walled off?
A
- coagulase (S. aureus): clots blood (converts fibrinogen > fibrin)
- staphylokinase (S. aureus): dissolves clot to allow bacterial spread
7
Q
which 3 enzymes do bacteria secrete that attack the host immune system?
A
- IgA protease (N. gonorrhoeae): cleaves IgA in mucosa
- DNAse: allows escape from neutrophil extracellular traps (NETs)
- enzymes that degrade complement proteins
8
Q
antigenic variation of bacteria
A
- continually changing the structure of their surface proteins and antigens so they avoid eliciting neutralising antibodies
- e.g. N. gonnorhoeae, salmonella
9
Q
how do bacteria achieve host mimicry?
A
- staph and strep bind to Fc region of antibody (instead of Fab) via protein A > X recognised by phagocytes
- bind to host ECM to avoid detection
- sticky, hydrated, polysaccharide capsule: mimic host polysaccharides to avoid detection
10
Q
mechanisms used by phagocytes to kill bacteria
A
- low pH
- enzymes e.g. lysosome
- reactive oxygen species e.g. H2O2
- reactive nitrogen species e.g. NO
- antimicrobial peptides e.g. defensives
- competitors: iron binding proteins e.g. lactoferrin
11
Q
how does opsonisation work?
A
- pathogen gets coated in antibody and/or complement (opsonins)
- this makes them taken up more readily by phagocytes
12
Q
3 ways that EXTRACELLULAR bacteria avoid uptake for phagocytosis
A
- release toxins to kill phagocyte
- prevent opsonisation by coating themselves in host antibodies via Fc region to look like self
- prevent contact w/ phagocyte e.g. via thick capsule
13
Q
3 ways that INTRACELLULAR bacteria avoid phagocytosis by hiding and thriving inside
A
- inhibit fusion of phagosome and lysosome by injecting T3SS effector proteins into host cell
- escape from phagolysosome into cytoplasm and replicate (can also go between cells via actin-mediated motility)
- resist killing by producing antioxidants e.g. catalase
14
Q
examples of facultative vs obligate intracellular bacteria
A
- facultative (can live inside or outside cells) - listeria, salmonella
- obligate (need to live inside) - chlamydia
15
Q
2 ways that bacteria invade non-phagocytic cells
A
- zipper mechanism: bacteria uses its adhesins on the host cell membrane to promote uptake of the bacteria (like a zipper)
- trigger mechanism: use molecular syringe (T3SS) to pump proteins into the cytoplasm to trick it into engulfing the bacteria by rearranging actin cytoskeleton
16
Q
shigella pathogenesis + Sx
A
- tricks gut epithelial cells into uptaking it into a vacuole
- hijacks cell’s actin to move between adjacent cells
- influx of immune cells creates gaps that the shigella can penetrate thru
- Sx: bloody mucoid diarrhoea, severe stomach cramps, dehydration and fever
17
Q
bacterial endo and exotoxins
A
- endotoxins: outer membrane of gram -ve bacteria contains LPS (toxic component is lipid A) which can overactivate immune mechanisms and cause septic shock (fever, blood clotting, weakness)
- exotoxins: protein toxins that are secreted (eg superantigens)
18
Q
sepsis vs septic shock
A
- sepsis: systemic inflammatory response to a microbial infection > can lead to organ failure and death
- septic shock: sepsis-induced hypotension that persists despite fluid treatment
19
Q
TIME acronym for sepsis
A
- T: body temperature
- I: signs and symptoms of infection
- M: mental decline
- E: extremely ill
- S: slurred speech
- E: extreme shivering, muscle pain or fever
- P: passing no urine all day
- S: severe breathlessness
- I: it feels like you’re going to die
- S: skin mottled or discoloured
20
Q
3 classes of exotoxins
A
- superantigens: bind to MHC II and TCR = activate T cells = cytokine storm = hypotension, toxic shock, organ failure e.g. S. aureus (toxic shock from tampons)
- toxins that target cell surface: phospholipases and pore-forming cytolysins
- toxins that modify intracellular targets: diphtheria, cholera, neurotoxins
21
Q
phospholipases and pore-forming cytolysins
A
- C. perfringens a-toxin: phospholipase C > hydrolyses membrane phospholipids to create an anaerobic environment = kill cells = gas gangrene
- cytolysins: punch holes in cell membrane to cause lysis (often in RBC) e.g. S. aureus alpha-haemolysins
22
Q
describe the structure of bacterial toxins which modify intracellular targets
A
- A/B structure
- A: enzyme which modifies intracellular target
- B: binds toxin to cell membrane and moves component A into cell
- simple A/B toxins: diphtheria
- compound A/B toxin: cholera
23
Q
diphtheria toxin
A
- infection of nasopharynx + tonsils (C. diphtheria)
- ADP-ribosyltransferase inactivates (EF2)
- prevents cells from making protein, cell necrosis
- inflammation & swelling that can obstruct airway
24
Q
cholera toxin
A
- acute food-borne infection of the GIT, caused by Vibrio cholerae
- AB5 toxin increases cAMP expression > uncontrolled electrolyte release
- diarrhoea, rice water stools, rapid fluid loss
25
describe the 2 neurotoxins from bacteria
- both are proteases, deadliest toxins known
- botulinum: blocks release of Ach > flaccid muscle paralysis (can't contract > can't breathe)
- tetanus (Cl. tetani): blocks release of inhibitory neurotransmitters glycine and GABA > rigid muscle spasms e.g. lock jaw
26
gram positive vs negative cell wall
- gram +ve (purple): thick peptidoglycan layer
- gram -ve (red): thin peptidoglycan layer with lipopolysaccharides on outside
27
bacteria shapes
- coccus = round
- bacili = rod-shaped
- spiral shaped
28
which bacteria can't be gram stained?
- when they have waxy unusual lipids and mycolic acid in cell wall > don't uptake gram stains
- e.g. mycobacteria
- need specialised staining - acid fast staining
29
4 specialised bacterial morphology
- flagella (made of flagellin protein): rotates like a propeller for motility
- hydrated sticky polysaccharide capsule: avoid phagocytosis, mimic human polysaccharides, adherence
- pili + fimbriae: hair-like projections for adhesion to host + surfaces + other bacteria
- endospores: 1 bacteria makes 1 heat resistant spore, allows it to persist in environment
30
how does binary fission occur
- chromosome duplicates
- cell elongates
- cleaves and splits into 2
31
strict aerobes
microaerophilic bacteria
- die w/o oxygen
- need low oxygen
32
facultative anaerobes
aerotolerant anaerobes
- can survive w/ or w/o oxygen
- can grow in but not killed by oxygen
33
strict/obligate anaerobes
- killed by oxygen
34
which common normal flora bacteria can also be the causative agent of nosocomial infections and skin infections e.g. boils and scalded skin syndrome?
staph aureus
35
key normal flora
- viridian strep
- candida
- staph aureus
- neisseria meningitidis
- enterococcus
- e coli
- lactobacilli
36
how does the method of birth impact the normal flora of the baby?
- babies born vaginally have more normal flora compared to C section
- get a lot of flora from vagina
37
most common nosocomial infection
UTI
38
One Health triad
- human health
- animal health
- environmental health
39
pan resistance
- when a microbe is resistant to all known antimicrobial therapies
40
consequences of not stopping antimicrobial resistance
- routine surgeries would be impossible
- many more deaths from infectious diseases
- return to the pre-antibiotic era
- burden on healthcare system
41
3 types of antibiotic resistance
- intrinsic resistance e.g. can't penetrate cell wall due to LPS, mycolic acid etc
- acquired resistance: mutations or horizontal gene transfer
- tolerance (non-genetic): sensitive to antibiotics but move away and appear to be resistant
42
how does antibiotic tolerance occur?
- bacteria can be walled off within abscess cavity > drug cannot
- remain dormant in tissue for many years > can't treat b/c inactive
- lose cell wall & survive as protoplast > insensitive to cell-wall-active drugs
- presence of foreign body e.g. implant, catheter > biofilm is hard to penetrate
43
4 methods of horizontal gene transfer
- transformation: bacteria uptake DNA from dead bacteria in ECF
- conjugation: transfer of plasmids b/n bacteria via sex pilus
- transduction: bacteriophage adds bacterial DNA into own genome and inserts into other bacteria cells
- transposons can carry resistance genes - these can jump between plasmids and bacteria
44
how do resistance genes actually make the bacteria resistant?
- produce proteins which modify or destroy antibiotic e.g. enzymes/toxins
- use efflux pump to get rid of the antibiotic
45
what is contributing to antimicrobial resistance?
- climate change: increases spread of infection
- overuse/incorrect use of antibiotics: humans and agriculture
- poor sanitation, pollution: create optimal conditions for microbes
- poor infection control and tracing
- lack of recognition that this is not just a healthcare problem (agriculture too)
46
how can a one health approach combat AMR
- tracking resistance patterns
- prevent infection > prevent spread e.g. hand hygiene, vaccination
- improve global use of antibiotics e.g. don't use human ones on animals, MIND ME creed
- address climate change effects
