1
Q
what are the structural features of streptococci
A
- they are gram-positive
- spherical or ovoid cocci (0.5-1 µm)
- grow in chains
- some streptococci have capsules
2
Q
how many species of streptococci are there
A
- > 30
- several are important human pathogens
3
Q
are streptococci susceptible to penicillin
A
most are
4
Q
what is a major type of streptococci
A
S. pyogenes or group A streptococcus
5
Q
how is S. pyogenes carried
A
asymptomatic colonisation of upper respiratory tract (≈ 20% carriers)
6
Q
how is S. pyogenes spread
A
- person-to-person spread by respiratory droplets
- wound infections
- crowding (e.g. classrooms)
7
Q
who carries S. pyogenes
A
- only humans!
- higher rates in Maori and Pacific Island populations
8
Q
how can you identify S. pyogenes in a lab
A
1) catalase test do distinguish between staphylococci and streptococci - streptococci will produce no bubbles
2) add the streptococci to a blood agar plate - only certain, including S. pyogenes, show complete/beta lysis
3) grow the beta hemolytic bacteria in a bacitracin agar plate - S. pyogenes is the only bacteria that is susceptible to bacitracin so a zone of inhibition will be observed
9
Q
what are the S. pyogenes virulence factors
A
- promote attachment to host cells (adhesins)
- help bacterium to enter host cell (invasins)
- secreted toxins that damage host cell or tissue (e.g. cytolysins)
- help bacteria to spread from local infection (spreading factors)
- over-stimulate immune response (immunopathogenic factors)
- mediate immune evasion
10
Q
examples of adhesins in S. pyogenes
A
- MSCRAMMS (microbial surface components recognising
adhesive matrix molecules) - pili
11
Q
examples of MSCRAMMS in S. pyogenes
A
- M protein: adhesin, antiphagocytotic
- F protein: binds fibronectin
- Cpa: collagen-binding protein
12
Q
describe pili in S. pyogenes
A
- long hair-like structures protruding from cell surface
- anchored to the bacterial cell wall
- help bacteria bind to host cell
- help bacteria to aggregate (and form biofilm)
13
Q
is pili found in both streptococci and staphylococci
A
no! only streptococci
14
Q
examples of cytolysins in S. pyogenes
A
- streptolysin O = SLO
- streptolysin S = SLS
- both are hemolysins
- both lyse leucocytes, erythrocytes and platelets
15
Q
describe streptolysin O
A
- a cytolysin
- oxygen-labile = gets inactivated by oxygen so works best in low-oxygen environments
- highly antigenic = immune system strongly recognises it
16
Q
describe streptolysin S
A
- a cytolysin
- oxygen-stable = works even when oxygen is present
17
Q
what is the significance of streptolysin O’s antigens
A
- since its is highly antigenic our body makes antibodies against it
- the antibodies can be measured through an ASO (anti streptolysin O) test
- this can be used to detect infection with S. pyogenes which is important for rheumatic fever
18
Q
what are the spreading factors of S. pyogenes
A
- streptokinase
- lipases
- nucleases
- hyaluronidase
- proteases
19
Q
what does streptokinase do
A
- S. pyogenes spreading factor
- our body tries to trap bacteria by clots
- streptokinase causes fibrinolysis (lyses blood clots), anti-coagulant
20
Q
what do lipases do
A
- S. pyogenes spreading factor
- hydrolyse lipids for bacterial invasion of skin (cutaneous tissue)
21
Q
what do nucleases do
A
- S. pyogenes spreading factor
- hydrolyses DNA for destruction of neutrophil extracellular traps
22
Q
what does hyaluronidase do
A
- S. pyogenes spreading factor
- hydrolyses hyaluronic acid in connective tissue
23
Q
what do proteases do
A
- S. pyogenes spreading factor
- streptococcal cysteine protease (SCP) breaks down a wide range of proteins
24
Q
examples of immunopathogenic factors in S. pyogenes
A
superantigens
25
what do superantigens do
- trigger massive release of pro-inflammatory cytokines
- this causes over-stimulation of immune response and systemic inflammation
26
superantigens in S. pyogenes vs S. aureus
in S. aureus they cause food poisoning, but not in S. pyogenes
27
example of immune evasion factors in S. pyogenes
- capsule (present only in some strains)
- M-protein
- C5a peptidase
28
what do capsules do
- S. pyogenes immune evasion factor
- hyaluronic acid coat
- inhibits phagocytosis
- made of hyaluronic acid which human cells recognise, so the bacteria can "hide"
29
what does M-protein do
- S. pyogenes immune evasion factor
- surface protein on the bacterial cell wall
- interferes with phagocytosis by preventing complement factor C3b from opsonising S. pyogenes
30
what does C5a peptidase do
- S. pyogenes immune evasion factor
- enzyme on the bacterial surface
- C5a normally attracts neutrophils to infection site
- C5a peptidase cuts C5a → neutrophils don’t get the signal
31
S. aureus vs S. pyogenes capsule
S. aureus does not produce hyaluronic acid like S. pyogenes, so it doesn't have the same camouflage effect as S. pyogenes does
32
what are the types of diseases caused by S. pyogenes
- non-invasive diseases
- invasive diseases
- post-streptococcal diseases
33
non-invasive diseases caused by S. pyogenes
- pharyngitis/tonsillitis
- pyoderma (impetigo)
- cellulitis
34
invasive diseases caused by S. pyogenes
- necrotising fasciitis (flesh-eating disease)
- streptococcal toxic shock syndrome
35
post-streptococcal diseases caused by S. pyogenes
- acute rheumatic fever
- acute glomerulonephritis
36
what kind of infection is impetigo
- a polymicrobial infection
- staphylococci and streptococci "team up" to cause the infection
37
describe pharyngitis
- caused by S. pyogenes
- develops 2-4 days after exposure to S. pyogenes
- can lead to scarlet fever
38
symptoms of pharyngitis
- sore throat
- fever
- reddened pharynx
- pus-filled vesicles on tonsils
39
what is scarlet fever
- a complication of pharyngitis
- can develop into a serious systemic disease
40
how does scarlet fever develop
- after S. pyogenes infection, pharyngitis/tonsillitis develops
- some strains produce SPE-A (scarlet fever toxin)
- SPE-A acts as a superantigen, causing a massive immune activation (however the S. pyogenes remains localised)
- the outcome is scarlet fever
41
symptoms of scarlet fever
- fever
- sore throat
- “strawberry tongue”
- characteristic rash on chest
42
what can pharyngitis/tonsillitis be treated with
penicillin, since streptococci are susceptible to it
43
describe impetigo
- a purulent infection of the skin
- caused by S. pyogenes colonisation after contact with infected person or object
44
how is impetigo spread
- spread to subcutaneous tissue (deepest layer of skin) through break in skin (e.g. scratch)
- easily spread, often in hot/humid climate
45
describe cellulitis
- infection of skin that involves subcutaneous tissue (deepest layer of skin), e.g. by a cut
- acute, rapidly spreading infections
46
describe necrotising fasciitis
- deep infection of the skin that involves destruction of muscles
- S. pyogenes is introduced through e.g. minor cuts, trauma, burn
- often develops into severe systemic disease with high mortality
47
how is necrotising fasciitis spread
it's spread into the deep tissue by spreading factors (DNAses, proteases, hyaluronidase)
48
describe streptococcal shock syndrome
- often follows necrotising fasciitis and sepsis
- mortality rate: 30-70% (more severe than staphylococcal TS)
49
what causes streptococcal shock syndrome
- massive release of pro-inflammatory cytokines in response to superantigen secretion
- overstimulation of immune response causes systemic inflammation
50
symptoms of streptococcal shock syndrome
- fever
- headache
- multiorgan failure and shock
51
describe rheumatic fever
- develops after untreated/chronic pharyngitis due to GAS
- autoimmune disease, NOT infection!
52
how does rheumatic fever occur
1) the immune system detects bacterial antigens (like M protein) and starts making antibodies
2) cross-reaction: an epitope of the M protein may be similar to an epitope in your own heart, joints, or other tissues
3) immune cells can't always tell the difference, so the antibodies begin to attack your own tissues
53
what is affected in rheumatic fever
- heart
- joints
- blood vessels
54
how is the heart affected in rheumatic fever
- inflammation of endocardium, myocardium, pericardium
- thickened and deformed valves
- granulomas (immune cell clusters) in myocardium
55
how are joints affected in rheumatic fever
- arthritis
- swelling
- pain
56
how are blood vessels affected in rheumatic fever
inflammation of vessels
57
describe how bacteria is normally phagocytosed
1) immune system coats bacteria with antibodies and complement - this is called opsonisation
2) neutrophils have receptors that bind Fc region of antibodies and C3b
3) they recognise the bacteria as foreign then engulf the bacteria into a phagosome
4) the bacteria is killed in the phagosome
58
describe how bacteria is phagocytosed in rheumatic fever
type II hypersensitivity
1) antibodies are produced against bacterial antigens, e.g. M protein
2) these antibodies also bind to host tissues (heart, joints) and now your own cells are mistakenly opsonised
3) host cells now have antibodies attached to them
4) ADCC: immune cells bind to antibodies on host cells, release toxic substances and kill the host cell
59
who is mostly affected by rheumatic fever
- children ages 4-16
- people from low-socioeconomic regions (due to overcrowding, damp rooms)
60
what's another group of streptococci
S. agalactiae or group B streptococci
61
how is S. agalactiae carried
- asymptomatic colonisation of upper respiratory & genitourinary tract
- vaginal carriage in 15-35% of adult woman
62
how is S. agalactiae most often spread to cause infection
acquired from mother during pregnancy, at time of birth or the first week after birth
63
what diseases can S. agalactiae cause
neonatal diseases:
- pneumonia
- bacteremia
- sepsis
- meningitis
64
what are the 2 types of neonatal diseases associated with S. agalactiae
- early-onset disease (EOD): acquired from the mother during birth
- late-onset disease (days to ~3 months). can be acquired from mother or from environment (hospital, caregivers)
65
what is viridans streptococci
- a large group of commensal Gram-positive streptococci
- they are α-hemolytic so produce a green colour on an agar plate
66
where is viridans streptococci found
- asymptomatic colonisation of oropharynx
- live in the mouth as commensal bacteria
67
what disease do viridans streptococci cause
- dental caries (tooth decay): S. mutans, S. sobrinus
- subacute endocarditis: S. gordonii, S. mitis
- septic shock in immuno-compromised patients
68
endocarditis in staphylococcus vs streptococcus
- in staphylococci it is acute, aggressive, and highly lethal
- in streptococci (viridans) it is typically subacute, slower-progressing
69
why do you get asked if you've had rheumatic fever when visiting the dentist
- viridans streptococci normally reside in the mouth
- during tooth extraction, gum bleeding, etc., these bacteria can enter the bloodstream
- once in the blood viridans can cause infective endocarditis
70
how can you identify viridans streptococci in a lab
1) catalase test do distinguish between staphylococci and streptococci - streptococci will produce no bubbles
2) add the streptococci to a blood agar plate - only certain, including viridans, show alpha lysis
3) grow the alpha hemolytic bacteria in a optochin agar plate - viridans strep is the only bacteria that is resistant to optochin so a zone of inhibition will *not* be observed
71
what's streptococci pneumoniae
- gram-positive diplococcus
- asymptomatically carried in the nose but can spread to other parts
72
who carries streptococci pneumoniae
- 30-65% of children are asymptomatic carriers
- <10% of adults are asymptomatic carriers
73
what are the streptococci pneumoniae risk factors
- young age
- sneezing, coughing
- close contact
- viral infections can make streptococci pneumoniae cause secondary infections (e.g. pneumonia)
74
what diseases can streptococci pneumoniae cause
- pneumonia, if aspired
- meningitis: via bacteraemia, the bacteria can travel to the brain and cause meningitis
- otitis media: middle ear infection
75
how does pneumonia develop through streptococci pneumoniae
1) after aspiration, bacteria from the upper respiratory tract get aspirated into the lungs
2) bacteria reach alveoli and multiply
3) neutrophils + macrophages flood in
4) the inflammation fills alveoli with fluids, making respiration difficult
76
symptoms of pneumonia
- fever
- yellowish sputum (phlegm)
- chest pain
medsci 202
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