Microbiology 1 - Staphylococci Introducation: Organism specific; aspects of classification. epidemiology, pathogenesis, diagnosis, treatment Epidemiology - is the study of how often diseases occur in different groups of people and why Lectures: Gram positive cocci: Staphylococci Anaerobic GPSFR (C.tetani) Mycrbacteria Antibiotics Gram negative facultative anaerobic rods Gram negative cocci; Neisseria Chlamydia Mycology Viruses: Retroviruses Parasites: Nematodes Directed Reading: Murray P. Medical Microbiology 6th edition, 2008 Lydyard P. Case Studies in Infectious Disease, Garland Science, 2010 Overviews: - Staphylococci: the beginnings of classification - Pathogenesis of Staphylococcus aureus infection - Methicillin resistant S. aureus (MRSA) - Vancomycin intermediate / resistant S. aureus (VISA / VRSA) - Clinical manifestations of S. aureus infection The Beginning Alexander Ogston (1881) - first description Classification of Staphylococci - Kingdom: Bacteria - Family: Staphylococcaceae (bunch of grapes) - Gram positive cocci: 0.5 - 1.0 um(micrometre) diameter - Facultative anaerobes; 18 oC - 40 oC o Anaerobe and aerobe - Catalase + o Breaks down hydrogen peroxide into ... - Approx 40 species; skin and mucous membranes
- Major differentiati Coagulate - fluid change to (semi)solid state Citrated Plasma - plasma mixed with sodium citrate, to COAGULASE PRODUCTION Ability to coagulate citrated plasma YES: Coagulate-positive staphylococci Staphylococci aureus NO: Coagulase-negative staphylococci (CNS) 30+ species; staphylococci epidermidis Staphylococci saprophyticus Listen to this part again S. Aureus Virulence (harmful) factors and mechanisms of pathogenicity . Ability to COLONISE the host and invade tissues . Ability to EVADE host defences . Ability to damage host through PRODUCTION OF INVASINS and EXOELLULAR TOXINS . (Ability to require RESISTANCE to antibiotics) o Not exactly a true virulence factor · Helps it live longer 2 Protein A Y- -1gG micro- capsule cell wall Invasins: hyaluronidase staphylysin- leukocidin leukotoxin- coagulase staphylokinase 3 Adhesins: cell- bound proteins 1 Toxins: TSST SE A- G. cell membrane damag toxic shock exfoliation emesis 3 fibrin fibronectin damaged tissue 1. Adhere to fibrin or fibronectin (damaged tissue) 2. Evade the host (using the capsule) 3. Exocellular Toxins a. TSST b. EFT c. SE-A-G Colonisation of host (ADHESINS) MSCRAMMS (Microbial Surface Components Recognising Adhesive Matrix Molecules) a) Expression of surface fibronectin and laminin binding proteins fibronectin, laminin (and fibrinogen) form the extracellular surface matrix of healthy endothelial and epithelial surfaces
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 They avoid host defences by; • CAPSULAR POLYSACCHARIDE · Stop components of the complement system to adhering to the skin of the invader • PROTEIN A (inhibits phagocytosis; immune 'disguise'; antibody 'sponge' · Inhibits IG-g · Antibody sponge that sticks it the wrong way round • LEUCOCIDIN production (Panton Valentine Leucocidin -PVL) pore-forming toxin; WBC destruction Listen to this part again Invasion of host tissue (INVASINS) Produces these invasins; · Membrane damaging toxins (eg. a-haemolysin -type II toxin -membrane) Damages that binds tp. The memvrame of the red blood cell and forms pores Type 2 - binds to membranes of