1
Q
what are the 3 clinically relevant staphylococci
A
- staphylococcus aureus (S. aureus)
- staphylococcus epidermidis
- staphylococcus saprophyticus
2
Q
what are the general characteristics of staphylococci
A
- irregular cell clusters (grape-like)
- gram-positive
- spherical (cocci)
- non-motile
3
Q
what are S. aureus resistant to
A
dry conditions and up to 10% NaCl (halodurent)
4
Q
where are S. aureus commonly found in a human body
A
- moist skin folds (like armpits)
- oropharynx
- gastrointestinal tract
- urogenital tract
5
Q
can you be a passive carrier for S. aureus
A
yes - 15% of normal healthy adults are persistent nasopharyngeal carriers
6
Q
what kind of pathogen is S. aureus
A
opportunistic pathogen
7
Q
how is S. aureus transmitted
A
human-to-human, via:
- contamination of dry surface
- splinters
- cracked/damaged skin
8
Q
what is a group of people with high rates of S. aureus carriage
A
hospital staff
9
Q
how does S. aureus react to penicillin
A
~90% of S. aureus is resistant to penicillin as they carry the B-lactamase gene
10
Q
how does S. aureus react to penicillin alternatives, like methicillin
A
there has been an emergence of methicillin resistant strains
11
Q
what are the steps to distinguishing between streptococci and staphylococci and further
A
1) do gram-staining: both strepto and staphylococci are gram positive
2) do a catalase test - staphylococci will produce bubbles
3) do a coagulase test - S. aureus is the only staphylococci that forms clots
12
Q
what’s a way other than a catalase test to distinguish streptococci and staphylococci and further
A
- growing both on mannitol salt agar
- staphylococci is halodurant so it will grow, while streptococci won’t
- S. aureus can also ferment sugar (mannitol), which will lower the pH and change the colour on the agar to yellow
13
Q
example of virulence factors
A
- promote attachment to host cells (adhesins)
- help bacterium to enter host cell (invasins)
- damage host cell or tissue (cytolysins)
- help bacteria to spread from local infection (spreading factors)
- over-stimulate immune response (immunopathogenic factors)
- mediate immune evasion
14
Q
adhesins in S. aureus
A
- produces MSCRAMMS: microbial surface components recognising adhesive matrix molecules
- proteins on the surface of the microbe that recognise and bind to ECM proteins
- each MSCRAMM is specific to its target, e.g. collagen MSCRAMM or fibronectin MSCRAMM
- important for colonisation
15
Q
cytolysins in S. aureus
A
- alpha-toxin or hemolysin: binds to the membrane of host cells and forms a pore (hole) in it, causing cell lysis (death)
- beta-toxin: hydrolysis of membrane phospholipids (sphingomyelins)
16
Q
why do bacteria produce cytolysins
A
- leukocytes: immune evasion
- erythrocytes: gaining access to iron and nutrients
- tissue cells: bacterial spreading
17
Q
what toxin do bacteria use to get access to iron
A
alpha-toxin, as it specifically causes hemolysis
18
Q
what’s a toxin that is only found in S. aureus
A
- exfoliative toxins: serine proteases that split the intercellular bridges (desmosomes) between cells
- this causes peeling of skin
19
Q
examples of spreading factors
A
- lipases: hydrolyse lipids
- nucleases: hydrolyses DNA
- hyaluronidase: hydrolyses hyaluronic acid
- proteases
- staphylokinase (fibrinolysin): causes fibrinolysis
20
Q
why do S. aureus have staphylokinase
A
- when a tissue is damaged, fibrin forms a clot which acts like a barrier to trap bacteria
- staphylokinase activates plasminogen → plasmin, which breaks down clots (fibrinolysis)
- the bacteria can dissolve the clot, escape the area where they were trapped and spread through tissue
21
Q
immunopathogenic factors in S. aureus
A
- normal: antigen-presenting cell (APC) displays a small antigen fragment on MHC II. very few T cells (0.001%) match that antigen and become activated = controlled immune response
- superantigen: bind to MHC II and physically link the APC and T cell together, activating the T cell (20%) even if it doesn’t recognize the antigen = massive immune response of cytokines
22
Q
what are the effects of superantigens on the body
A
- amplified immune response due to T-cell activation and cytokine release
- many enterotoxins are also superantigens, and they can cause food poisoning
23
Q
examples of immune evasion factors
A
- capsule
- slime layer
- catalase
- clumping factor ClF-A
- protein A
24
Q
capsule role in bacteria
A
immune evasion factor
- dense polysaccharide coat
- prevents opsonisation
- inhibits phagocytosis
- contains water which protects bacteria against drying out
25
slime layer role in bacteria
immune evasion factor
- loose-bound water-soluble film (biofilm)
- made from secreted polysaccharides
- protects from immune factors and antibiotics
- sticks them to a surface
26
what's a medical issue with biofilm
antibiotics cannot penetrate and destroy it when it falls on indwelling catheters, so the whole device must be removed from the patient
27
catalase role in bacteria
immune evasion factor
- enzyme produced by S. aureus
- detoxifies peroxides produced by macrophages and neutrophils to try and destroy pathogens
- 2H2O2 --> 2H2O + O2
28
clumping factor ClF-A (coagulase) role in bacteria
immune evasion factor
- binds fibrinogen and converts it into insoluble fibrin
- the clot coats the bacteria making it harder for antibodies and phagocytes to attack
- multiple bacteria can stick together in this fibrin "shield" forming clumps
29
protein A role in bacteria
immune evasion factor
- surface protein on most S. aureus strains
- binds IgG, flipping the antibody around
- phagocytes can't recognise the antibody and phagocytosis is blocked
30
what diseases can staphylococci cause
- superficial skin disease
- invasive diseases
- toxigenic diseases
31
give an example of a superficial skin disease
impetigo: localised cutaneous (skin) infection with pus-filled vesicles. primarily effects children
32
what skin infections does S. aureus cause
cutaneous purulent skin infections
33
examples of cutaneous purulent skin infections
- impetigo: localised cutaneous (skin) infection with pus-filled vesicles. primarily effects children
- folliculitis: impetigo involving hair follicles
- furuncles or boils: painful pus-filled cutaneous nodules
- carbuncles: merging of furuncles, extension into subcutaneous tissue can lead to systemic disease
34
what is folliculitis
cutaneous purulent skin infection that is impetigo involving hair follicles
35
what are furuncles or boils
cutaneous purulent skin infection that are painful pus-filled cutaneous nodules
36
what are carbuncles
- cutaneous purulent skin infection that are the merging of furuncles
- extension into subcutaneous tissue can lead to systemic disease
37
what's an eye infection caused by S. aureus
corneal ulcer
- deep infection of the cornea after abrasion, e.g. contact lenses
- can also be caused by several other bacteria, viruses and fungi
38
what's a lung infection caused by S. aureus
pneumonia
39
how can S. aureus pneumonia be contracted
- by inhaling saliva or mucus
- by bacteria travelling through the bloodstream from another infection site
40
how does S. aureus damage the body during pneumonia
- releases cytolytic toxins that can cause consolidation and abscess formation in lungs
- severe form is necrotizing pneumonia: lung cells are dissolved due to cytolytic toxins
41
what's a bone infection caused by S. aureus
osteomyelitis
- comes together with septic arthritis!
42
how can osteomyelitis be contracted from S. aureus
- hematogenous spread: through the bloodstream from another site of infection
- secondary infection from trauma: direct introduction of bacteria after fractures, surgery, or open wounds
43
who does osteomyelitis affect most
children
44
is osteomyelitis easily treated
yes, with the right antibiotics
45
what's a joint infection caused by S. aureus
septic arthritis
- comes together with osteomyelitis!
46
how can joint infection be contracted from S. aureus
- hematogenous spread: through the bloodstream from another site of infection
- direct introduction: via intra-articular injections, joint surgery, or trauma - bacteria are introduced directly into the joint space
47
what does septic arthritis do to your joints
- the joint fills with pus and causes pain
- the joint fluid gets a milky, yellowish colour instead of its normal clear
48
what's a heart infection caused by S. aureus
acute endocarditis
49
how can acute endocarditis be contracted from S. aureus
- spread of bacteria into the blood from a focus of infection
- >50% of cases are from contaminated catheters or surgery in a hospital
50
what does acute endocarditis do to your heart
1) damages endothelial lining of the heart valve, forming a structure called a vegetation
2) vegetation contains bacteria, platelets and cellular debris
3) S. aureus secretes enzymes and toxins that destroy tissue, causing valve dysfunction
4) septic emboli: pieces of the vegetation can break off and travel through the bloodstream, causing infections in other parts of the body
51
what's the mortality rate for acute endocarditis
50%
52
examples of toxigenic diseases caused by S. aureus
- staphylococcal food poisoning
- staphylococcal scalded skin syndrome
- toxic shock syndrome
- menstrual toxic shock syndrome
53
describe staphylococcal food poisoning
- most common foodborne illness
- microbial intoxication, not infection
54
how does one contract staphylococcal food poisoning
- contamination of food by human carrier and improper food handling
- caused by heat-stable enterotoxins
55
symptoms of staphylococcal food poisoning
- severe vomiting, diarrhea, abdominal pain, nausea, sweating headache
- rapid onset (hours), generally lasting for less than 24h
56
describe staphylococcal scalded skin syndrome
- cutaneous blisters followed by shedding of epithelium
- affects primarily neonates and young children
- low mortality rate due to development of immunity (not life-threatening)
57
what causes staphylococcal scalded skin syndrome
exfoliative toxins
58
describe toxic shock syndrome
1) caused by growth of a superantigen-producing S. aureus strain at a local site
2) toxins enter the bloodstream and act as superantigens leading to large amounts of pro-inflammatory cytokines
3) this cytokine release results in systemic disease
59
symptoms of toxic shock syndrome
- fever
- hypotension
- erythematous rash
- intravascular coagulation
- multiple organ failure
60
describe menstrual toxic shock syndrome
- occurs when S. aureus grows in the vagina and produces TSST which is a superantigen that can penetrate mucosal barrier
- caused by prolonged use of expandable tampon
61
what are MSSAs
- methicillin-susceptible staphylococcus aureus
- MSSA can be killed by β-lactam antibiotics that are resistant to β-lactamase - penicillin is not resistant!
62
what are MRSAs
- methicillin-resistant S. aureus
- the bacteria are resistant to β-lactam antibiotics, even those resistant to β-lactamase
63
what does penicillin/amoxicillin treat best
- streptococcus pyogenes
- most S. aureus are resistant
64
what does augmentin or flucloxacillin treat
- streptococcus pyogenes
- MSSA
- not effective against MRSA
65
what is vancomycin used to treat
- MRSA
- avoid using for MSSA as they can gain resistance then
- last resort drug
medsci 202
flashcards
Decks in class (13)
# Cards
