breaks down hydrogen peroxide into water and oxygen, bubbles (protects from oxidative burst from phagocytic cell)
catalase reaction test
staphylococci = positive, streptococci = negative
CoNS
generally low virulence pathogens that don't cause disease, most normal skin flora
coagulase test
for staphylococci, test for production of coagulase enzyme (positive only in s.aureus) which coagulates plasma otherwise spread across tube
when will CoNS cause disease
skin barrier breached by invasive devices or in infants
2 CoNS example
s.epidermidis and s.saprophyticus
how many people carry s.aureus and where
20-40% population, groin, nostrils and armpits
s.aureus infection
localised or disseminated infection, pyogenic (pus forming - abscess) infections in most organs
coagulase toxin (s.aureus)
walls off infection while lytic toxins destroy tissue
quorum sensing
chemical communication between bacteria that depends on the surrounding environmental conditions, including bacterial density (more = more talk)
QS influences bacterial behaviour, allowing bacteria to collaborate in response to environmental conditions
how QS system works in s.aureus
though accessory gene regulator (agr), contributes to pathogenicity in several infection types (transition from colonisation to disease, will it become a pathogen or commensal) - subcutaneous abscesses, endocarditis
toxin producing strain s.aureus cause non pyogenic disease
staphylococcal scalded skin syndrome (SSSS)
staphylococcal toxic shock syndrom (STSS)
staphylococcal food poisoning
superantigens
bypass normal antigen presentation by directly cross linking TCR and MCH2 causing polyclonal activation of broad range of TCRs, no specificity in reaction(binds outside presenting cleft)
SSSS
caused by an enterotoxin (a super antigen) the gene acquired a bacteriophage via transduction, causes layers of skin to peel off
enterotoxin
harms digestive system
beta hemolysis
blood is dissolved, agar transparent (enzyme breaks down RBC)
alpha hemolysis
partial haemolysis od agar
gamma hemolysis
no hemolysis
B haemolytic strep classification
according to antigenic differences in cell wall carbs (Lancefield system A-H, K-V)
2 lancefield groups significance
group A (step A) = streptococcus pyogenes
group B = streptococcus agalactiae
a - haemolytic streptococci
common commensal of upper respiratory, gut, genital tract
2 groups of a haemolytic streptococci
1 - streptococcus pneumonia 2 - viridans group of strep (includes strep mutants group)
streptococcus pneumoniae
gram positive diplococcus, leading bacterial cause of pneumonia, also cause meningitis
streptococcus pneumoniae capsule
more than 94 types, pathogenic factor
streptococcus pneumoniae vaccine
protection to specific capsular type (serotype), common vaccine targets 13
S.pneumoniae carriage
nasopharyngeal carriage needed for transmission of bacteria and precedes invasive disease, carriage common in children (usually through mucus membranes)
evolution of s.mutans
acquired gtf gene via horizontal gene transfer from lactic acid bacilli, selected for this because could catabolise sugar
polysaccharide vaccines problem
based on bacterial capsules, they don't induce strong or persistent immune response in young children, only stimulate B cells not T cells. B cells just die, don't produce memory B cells
conjugate vaccines
polysaccharide linked to a carrier protein molecule
why are conjugate vaccines better
induce memory responses and reduce nasopharyngeal carriage of bacteria (impact transmission), stimulates B and T cells and produce memory B cells/antibodies
primary infection sites of strep A infection (pyogenes)
throat (pharyngitis and tonsillitis) or skin (impetigo or cellulitis)
complications of strep A throat infection
abscess
complications of strep A skin infection
necrotizing fascitis (rapid tissue breakdown)
non suppurative complications strep A infection (pyogenes)
throat - acute rheumatic fever (can lead to heart disease)
skin - renal disease
acute rheumatic fever syndrome (following strep A)