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
Q
describe the 2 neurotoxins from bacteria
A
- 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
Q
gram positive vs negative cell wall
A
- gram +ve (purple): thick peptidoglycan layer
- gram -ve (red): thin peptidoglycan layer with lipopolysaccharides on outside
27
Q
bacteria shapes
A
- coccus = round
- bacili = rod-shaped
- spiral shaped
28
Q
which bacteria can’t be gram stained?
A
- 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
Q
4 specialised bacterial morphology
A
- 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
Q
how does binary fission occur
A
- chromosome duplicates
- cell elongates
- cleaves and splits into 2
31
Q
strict aerobes
microaerophilic bacteria
A
- die w/o oxygen
- need low oxygen
32
Q
facultative anaerobes
aerotolerant anaerobes
A
- can survive w/ or w/o oxygen
- can grow in but not killed by oxygen
33
Q
strict/obligate anaerobes
A
- killed by oxygen
34
Q
which common normal flora bacteria can also be the causative agent of nosocomial infections and skin infections e.g. boils and scalded skin syndrome?
A
staph aureus
35
Q
key normal flora
A
- viridian strep
- candida
- staph aureus
- neisseria meningitidis
- enterococcus
- e coli
- lactobacilli
36
Q
how does the method of birth impact the normal flora of the baby?
A
- babies born vaginally have more normal flora compared to C section
- get a lot of flora from vagina
37
Q
most common nosocomial infection
A
UTI
38
Q
One Health triad
A
- human health
- animal health
- environmental health
39
Q
pan resistance
A
- when a microbe is resistant to all known antimicrobial therapies
40
Q
consequences of not stopping antimicrobial resistance
A
- routine surgeries would be impossible
- many more deaths from infectious diseases
- return to the pre-antibiotic era
- burden on healthcare system
41
Q
3 types of antibiotic resistance
A
- 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
Q
how does antibiotic tolerance occur?
A
- 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
Q
4 methods of horizontal gene transfer
A
- 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
Q
how do resistance genes actually make the bacteria resistant?
A
- produce proteins which modify or destroy antibiotic e.g. enzymes/toxins
- use efflux pump to get rid of the antibiotic
45
Q
what is contributing to antimicrobial resistance?
A
- 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
Q
how can a one health approach combat AMR
A
- 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
