This document summarizes various gram-positive cocci bacteria including Staphylococci and Streptococci. It describes their pathogenicity, virulence factors, and ability to cause opportunistic infections. Key points mentioned are that S. aureus and S. intermedius are pyogenic bacteria that can cause disease when access sterile sites or in immunocompromised individuals. They produce various toxins and express surface proteins that contribute to their pathogenicity. Transmission is usually through direct contact or aerosols between hosts as they commonly reside on skin and mucosal surfaces.

1. GRAM +ve Bacteria: COCCI
BACTERIA STAPHILOCOCCI STREPTOCOCCI
VIRULENT OPORTUNISTIC TONSIL GENITAL TRACT BOVINE MAMMARYGLAND INTESTINE
S.aureus (biotypes: A-D)
S.(pseud)intermedius (E-F)
(and S.hyicus*)
S.epidermis
S.capitis
S.xylosus
S.pyogenes (A)
S.equi (C)
S.suis
S.canis (G)
S.zooepidemicus
Group B strep.c
S.agalactiae Faecal
strep.c
PATHOGENESIS S.a & S.i = pyogenic
Cell leakage= necrosis
Causediseasewhen access sterile
site/ableto grow due to reduced
immunity (immunocompromised)
Display multipleantibiotic
resistance
Classified on haemolysis on blood agar:α, β, γ
- Pyogenic (pus forming): *A, B, C, D and G
- Viridans (greening) – oral – non-pathogenic (S.salvarius)
- Enterococci (faecal)
- Lactic (found in milk etc) – milk scour (S.lactis)
*Lancefield grouping(20): based on carbohydratecell wall
TOXINS Haemolysins: α-toxin (S.a; S.i) = zone of β-haemolysis
β-toxin: wider zone of RBC change (sphingomyelin -> ceramide)
Leucocidins: Panton-ValentineLeukocidin (S.a)
TSST-1: superantigen (TCR-MHC II),cytokine over-production (TNFα)
Enterotoxins: Protein & heat liable;superantigens
Proteases, hyaluronidase, lipases: Digestive enz: tissuedestruction
Exfoliative toxins: blistering(humans/infants) (S.a)
Digestive enzymes toxic to mammalian cells:digestproteins & lipids =aa nutrition
Streptolysin O: haemolysin;inactivated by O2 (A,B,C,F and G)
Streptolysin S: haemolysin;O2 stable
Hyaluronidase: hydrolysishyaluronic acid of CT (A,B,C and S.suis)
Streptokinase: lyses fibrin clots breakingdown fibrin barrier = spread (A, C and G)
CELL-SURFACE
ASSOCIATED
PATHOGENICITY
DETERMINANTS
Fibronectin-binding proteins: adhere and colonise(S.a)
Fibrinogen-BP: adhere fibrin in wounds,coatin host-protein
Protein A: Bind Fc of IgG. Fab free to bind Ag, but IgG can’t activate
complement = C3b deposition = Anti-opsonin (S.a)
Capsule: inhib phag-opsin (inhib complement activation)
Intracellular survival: multiply in leukocytes=persistfollowing
treatment and apparentrecovery! (resume infection and disease:o)
Hyaluronic acid capsule (non-antigenic and antiphagocytic)
M-protein: fibrillarstructures;antiphagocytic
(A and C)
SPREAD Normally commensals of SKIN and MUCOUS MEMBRANES of UPPER
REST TRACT and INTESTINAL TRACT
Found in normal flora of animals (UPPERRESP TRACT and GUT)
Those that arephagocytosed are killed insidethe phagocytic cell
CHARACTERISTICS/
STERILISATION
Grow in bunches
Facultativeanaerobes
Metabolically active
Intracellular
Grow in chains
Do not immediately separate into individual daughter cells
Usually aerotolerant(Peptostreptococcus = strictanaerobes)
Survival outsidebody is poor: liveon host w/abundant nutrients
Extracellular*except S.suis
TRANSMISSION Proteases,hyaluronidase,lipases:spread and nutrition Direct contact/aerosol
DIAGNOSIS Catalase(DNase)+ve
Coagulase+ve (bound
coagulase)
S.hyicus: Catalase(DNase)+ve
But Coagulase–ve
Catalase(DNase) +ve
Coagulase–ve
Adheres to plastic
Catalase–ve = Do not splitH2O2 (no O2 release)
Whilecan be most aggressivepathogens; β-haemolytic strep.c of Lancefield groups
A,C and G remain sensitiveto Penicillin Gand other penicillins.
Resistanceunknown/