Lecture 6 - Streptococci and disease Flashcards
what are the general features of streptococci?
they are gram positive cocci
- they grow in chains
- some have capsules
- >30 species, several are important human pathogens
- most are still susceptible to penicillin
what is group A streptococcus most commonly known as?
streptococcus pyogenes
describe the epidemiology of streptococcus pyogenes
- asymptomatic colonisation of the upper respiratory tract (20% carriers)
- exclusively in humans
- wound infections also
how can we do a diagnostic for streptococcus pyogenes?
- gram stain -> gram +ve cocci
- catalase test -> no bubbles
- Blood agar -> beta hemolysis
- kirby bauer semi quantitative bacitracin susceptibility test -> sensitive
true or false, streptococci have the same general virulence factors as staphylococci
true
describe the MSCRAMMS of streptococci
MSCRAMMS
- M protein (antiphagocytotic)
- F protein (binds fibronectin)
- Cpa (collagen binding protein)
what adhesin do streptococci have that staphylococci dont?
pili
- hair structures that are cell wall anchored
- provides distance, basically just as adhesion on a stalk
- involved in biofilm formation
what cytolysins does streptococci have?
- streptolysin O (oxygen-labile)
- streptolysin S (oxygen stable)
how are the toxins in streptococci and staphylococci similar?
they can both do immune evasion by lysing cells of the immune system like WBCs
streptolysin O is highly antigenic. What does this mean?
- this streptolysin triggers a strong immune response and lots of anitbodies are made, but dont last very long
how can we see if a patient had a recent strep infection if the bacteria is no longer present?
- by looking at SLO titres. If the titre is very high, then the patient had recent GAS infection (group A strep)
what are the five main spreading factors?
- streptokinase (unique to strep)
- lipases
- nucleases
- hyaluronidases
- proteases
true or false, the streptokinase has the same mechanism as staphylokinase, but is unique to streptococci
true
what are the superantigens of streptococci?
- trigger massive release of pro-inflammatory cytokines
- over-stimulation of immune system
- doesn’t cause food poisoning
what are the 3 immune evasion factors of streptococci?
- capsule
- M-protein
- C5a peptidase
how is a capsule an immune evasion factor in streptococci?
- hyaluronic acid coat causes a camouflage effect, the immune system thinks it is self.
- capsule also prevents AB access to the cell surface
how is an M-protein an immune evasion factor?
- antiphagocytic
- prevents complement factor C3b from opsonising GAS
how is C5a peptidase an immune evasion factor?
cleaves complement factor C5a (neutrophil chemotaxis) and prevents neutrophils from migrating to site of infection (dont know where to go)
what are the three types of disease that streptococci cause?
- non-invasive disease
- invasive disease
- post-streptococcal disease
what non-invasive diseases can streptococci cause?
- pharyngitis, tonsilitis
- impetigo/pyoderma
- cellulitis
what invasive diseases can streptococci cause?
- necrotising fasciitis (flesh eating disease)
- streptococcal toxic shock syndrome
what post-streptococcal diseases can streptococci cause?
- acute rheumatic fever
- acute glomerulonephritis
what are post-streptococcal diseases?
they are not infections, but auto-immune reactions
what disease feature does streptococci not have, but staphylococci do have?
toxigenic diseases
so streptococcus pyogenes doesn’t cause microbial intoxication like staph aureus does with food poisoning
what is pharyngitis and tonsilitis?
- develops 2-4 days after exposure to S. pyogenes
- sore throat, fever, reddened pharynx, pus-filled vesicles on tonsils
what is scarlet fever?
- strep that is not treated produces pyrogenic exotoxin A, which is a superantigen
- GAS stays in the mouth, but the toxins spread and cause systemic disease
- fever, sore throat, strawberry tongue, rash on chest
how does impetigo happen with S. pyogenes?
- colonisation and spread to subcutaneous tissue after contact with infected person through a break in the skin barrier
what is cellulitis?
- an infection of the skin that involves subcutaneous tissue
- acute infection, so rapidly spreads via spreading factors such as hyaluronidase
what is necrotising fasciitis?
- deep infection of the skin that involved destruction of muscles, which is achieved through spreading factors
- often development into severe systemic diseases with high mortality
what are the ways S. pyogenes can enter and cause necrotising fasciitis?
- minor cuts
- trauma
- burn
- surgery
- vesicular viral infection
what is streptococcal toxic shock syndrome?
- often follows necrotising fasciitis and sepsis
- mortality rate is higher than Staphylococcal toxic shock
- superantigen secretion leads to overstimulation of immune response
what is rheumatic fever and rheumatic heart disease?
- develop after untreated sore throats due to GAS
- inflammation of heart components and joints (arthritis) and blood vessels
- not an infection but an autoimmune disease
what is the mechanism of rheumatic fever and rheumatic heart disease?
molecular mimicry
- GAS M protein has an epitope which is also present in the host cardiac myofibril, and so some of the antibodies cross-react to attack host cells
true or false, molecular mimicry of rheumatic heart disease occurs because some of our antibodies attack both S. pyogenes’ M protein and ours also.
false, we do not have an M protein. we just contain the same epitope in our cardiac myofibrils that bacteria have on their M proteins
do all our antibodies cross react during acute rheumatic heart disease?
no, only the ones targeted to the one specific epitope out of many epitopes and antibodies. so most will pass through the heart via the blood and not bind epitopes.
what type of reaction do cross-reactive antibodies trigger?
a type II hypersensitivity reaction
(Antibody-dependent cell-mediated cytotoxicity) (ADCC)
who are most at risk for rheumatic fever?
children aged 4-16, and people from low socioeconomic regions (overcrowded houses, damp rooms - high GAS infection rates)
what are group B streptococci also known as?
streptococcus agalactiae
what is the epidemiology of GBS
- asymptomatic colonisation of upper respiratory
- asymptomatic colonisation of genitourinary tract, but becomes a problem for the baby
- most infections in newborns are acquired from mother during pregnancy, birth or the first week after birth
what diseases stem from S. agalactiae?
neonatal disease:
- pneumonia
- bacteremia
- sepsis
- meningitis
streptococci grow in?
chains
what is the epidemiology of Viridans streptococci?
- asymptomatic colonisation of oropharynx
- commensales of the mouth flora
what disease comes from viridans streptococci?
- dental caries
- subacute endocarditis
- septic shock in immuno-compromised patients
what are the common viridans streptococci?
S. mutans
S. sobrinus
S gordonii
S mitis
which viridans strep cause dental caries?
S. mutans and S sobrinus
which viridans strep cause subacute endocarditis?
S. gordonii and S mitis
what is the diagnostic for S. viridans?
- gram stain, +ve cocci
- catalase test, negative
- blood agar - alpha hemolytic
- kirby bauer agar with optochin antibiotic, -> resistant
which strep is sensitive to optochin?
S. pneumoniae
describe the features of S. pneumoniae
- gram positive diplococcus
- most children are symptomatic carriers
- risk factors include young age, close contact and viral infections
State the diseases of S. pneumoniae
pneumonia
meningitis
bacteremia
sinusitis and otitis media (middle ear infection)
describe pneumonia
- bacteria multiply in alveoli
- most damage caused by immune response
describe meningitis
headache, fever, sepsis
- high mortality
- often leads to bacteremia
describe sinusitis and otitis media
occurs after viral infection
how can we do a diagnostic for streptococcus progenies?
