Lecture 1 - Staphylococcus Flashcards
(37 cards)
Which surgeon noticed some post surgical infections. In absecesses recover adn visualise organisms to look like bunches of grapes
William Ogston 1881
First description of staph
3 years after Ogston what did anton rosenbach do
Classify organisms from absseces into two groups - golden colonies on agar and smaller white colonies
Can s.epidermidis cause disease
No it is non pathogenic
What is the size of the staphylococci
0.5-1 um
Is staphylococcus catalase + or negative
Catalase positive
Are staphylococcus aerobic or anaerobic
FACULTATIVE ANAEROBE
What can differentiate s aureus from other staph
Coagulase positive
What does s aureus do with coagulase
Coagulate CITRATED PLASMA
CONVERT FIBRINOGEN TO FIBRIN - SURROUND ORGANISM WITH HUGE FIBRIN CLOT FOR PROTECTION FROM ANTIBIOTICS ETC
Name the three main virulence factors that staph areus has (basic)
1- adhesins - cell bound proteins (ATTACHMENT)
2- Protein A and microcapsule (EVASION)
3- Toxins and Invasins (DAMAGE HOST)
Name the three toxins produced and what effect they have
- TSST
- EFT
-SE A-G
Enterotoxins so cause vomiting.
Cause toxic shock( multifunction organ failure), exfoliation (skin blistering) and emesis (vomiting)
What antibody binds to protein A
IgG
Describe in detail how staph aureus colonise host
MSCRAMMS - microbial surface components recognising adhesive matrix molecules
A) expression of surface fibronectin and laminin binding proteins -
Fibronectin, laminin (and fibrinogen) form extracellular surface matrix of HEALTHY endothelial and epithelial surfaces (hence carriers of s.aureus if can bind to healthy tissue)
B) Expression of fibrin/fibrinogen binding proteins (clumping factor) - promotes adhesion to DAMAGED tissue and BLOOD CLOTS.
C) Expression of collagen binding protein - promotes adhesion to SEVERELY DAMAGED tissue. Collagen deeper in tissue.
In detail how does staph aureus evade host defences
CASPSULAR POLYSACCHARIDE - aka microcapsule.
Protein A - prevent c3b of complement attaching to surface of bacteria so prevent complement associated oxidation phagocytosis. It binds IgG WRONG WAY ROUND via Fc receptor instead of FAB
Leucocidin - pore forming toxin. protein toxin burst open wbc . Genes carried by bacteriophage injected into staph chromosome. PVL (Panton Valentine - Leucocidin) can burst open cell
What % carry lethal form of leucocidin
1-2%
How does staph aureus invade tissue
- membrane damaging toxins (alpha - haemolysin - type II toxin attack membrane )
- coagulase - clotting protective layer
- staphylokinase - fibrinolysis; bacterial spread (break down clot so can spread through tissue)
- hyaluronidase -lyses hyaluronic acid (as ECM make up of HA - can spread through ECM now)
- DNAase - split for nutrition
- Fatty Acid Modifying enzyme (FAME) - converts bacterial FA in infected tissue to alcohols e.g. Cholesterol
What are the enterotoxins produced by 60-70% of s aureus
A-E, G-J
Toxins INGESTED through contaminated food stuffs (custards, pastries, milk )
- food poisoning (profuse vomiting)
-HEAT STABILE at 100 deg for several minutes. S aureus may die but toxin live
What does the toxin TSST-1 do that some s aureus produce
Toxic shock syndrome toxin (TSST-1)
- toxins produced systemically
Associated with tampon use early 80s
Fever, shock, skin rash , multi system involvement
Carry sa in genital tract so don’t change tampons get this
What does exfoliative toxin do that some s aureus produce
Exfoliative A and B (ETA and ETB)
Toxins produce systemically (serine proteases split dermal junctions in skin and cause severe blistering. May start as little pimple lead to big blistering. )
- hence SCALDED SKIN SYNDROME
The s aureus exotoxins (enterotoxins A-E, G-J, TSST-1 and exfoliative toxins) are all superantigens. What does this mean
They all bind non specifically to MHC class II of antigen presenting cells
- AVOID DIGESTION PROCESS
- As it is non specific massive amount of t cells so increased cytokine release TNF, interleukins, get INF = toxic shock.
TYPE I TOXINS
What is the difference in ratios of t cell activation for normal antigen and super antigen
Normal - 1:10,000 T cells activated
Superantigen - 1:5 T cells activated
Briefly describe mrsa history
Methicillin a beta Lactam antibiotic introduced in 1960 to withstand beta lactamase producing staph
- MRSA: first described in 1961 ; recognised as a hospital pathogen in 70’s - rapid spread through hospitals 1980-2005
- if found in hospitals it is HA-MRSA if found in community, healthcare workers, and patients then (CA-MRSA)
- transmission patient to patient, environment to patient and HCW. To patient
What percentage of s areus are now mrsa
50%
How does s aureus become mrsa
MecA gene incorporated on SCCmec gene (staphylococcal cassette chromosome mec)
Encodes for additional pencilling binding proteins (PBP2a) ; reduced affinity for beta lactams
MRSA resistant to all beta lactam antibiotics
What is drug of choice for mrsa
Vancomycin - drug of choice - glycopeptide bind to D-ala D-ala. work at membrane level. Blocks action of transglycosidase and PBP enzymes (transpeptidase)
Prevent new wall subunits being added
