Gram Positive Cocci

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Staphylococcus Types (from the slides), normal flora etc.

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Aureus - MOST COMMON; skin diseases; food poisoning
Epidermidis - endocarditis, infections of catheters and implants
Saprophyticus - urinary tract infections
S. Aureus (nose) S. epidermidis (skin)
S. Saprophyticus (urinary Tract infections)
Major source of nosocomial infections
Can be resistant to penicillin (Methicillin resistant S. Aureus)
DONT FORGET OPPORTUNISTIC (hence the nosocomial infections)

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How is staph aureus different from the others?

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Coagulase production and hemolyzes blood (beta hemolysis shows up yellow)

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Important properties of Staph?

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1. Protein A: major protein in cell wall that binds Fc portion of IgG preventing complement.
2. Teichoic Acid: Antibodies can form to certain staph infectinos (e.g. endocarditis)

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Pathogenesis of Staph?

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Enterotoxin: acts on enterocytes in small intestine (usually involving an increase in cAMP). Usually heat resistant and is a result of release of Interleukin 1 & 2
Toxic Shock Syndrome Toxin: Also stimulus of interleukin 1 & 2 (produced by strains of S. Aureus) Toxin binds to class II MHC which then interacts with beta portion of T cell to stimulate release of interleukins.
Exfoliatin produced by phage group II producing scalded skin syndrome in children.
Leukocidins (alpha toxin) marked necrosis of tissue and skin and hemolysis.
(DONT FORGET AUREUS PRODUCES COAGULASE)

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Clinical Findings of Staph Aureus:

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skin infections, impetigo (pus filled blisters), furuncles, cellulitis
Bacteremia from localized lesion (can lead to endocarditis) *prosthetic valve endocarditis often caused by S. Epidermidis
Osteomyelitis
Pneumonia (post-op or following viral resp infection)
abscesses
Food Poisoning (enterotoxin)
TSST (fever, rash, hypotension)

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Lab Findings

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Gram positive!!! Staph Aureus is beta hemolytic (while the others show no hemolysis). Staph Aureus is coagulase positive.

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Streptococcus types:

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Pneumoniae
Pyogenes
Agalacticae
faecalis
bovis
Viridans group

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Important properties of Streptococcus:

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Beta/non-beta hemolytic (alpha or none)
C Carbohydrate: determines the group of beta hemolytic streptococci. This carbohydrate can inhibit lysozyme.
M Protein: anti phagocytic

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What is the difference between alpha and beta hemolyis?

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Green (alpha) indicative of partial hemolysis versus yellow/clear with complete hemolysis of the cell.

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Name beta hemolytic streptococci

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Pyogenes
Agalactiae
Faecalis (alpha or beta or none)

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S. Pyogenes Properties

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GROUP A streptococci and is important for humans--causes pharyngitis. Adhere to epithelium via pili and have lipoteichoic acid (remember gram positive cocci). BACITRACIN SUSCEPTIBLE
*Hemolysins S and O, responsible for strep throat (S oxygen stable toxic to tissue leukocytes and RBCs, O oxygen Labile, binds cholestrol, toxic to heart, and other tissues.)
*Erythrogenic toxin--scarlet fever rash and a superantigen that stimulates non specifically T-cells
*TSST Exotoxin A
*Exotoxin B necrotizing fasciitis ("flesh eating")

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S. Agalactiae properties:

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GROUP B streptococci that inhabits female genital tract and cause neonatal meningitis and sepsis. BACITRACIN RESISTANT

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S. Faecalis

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Group D Strep. (ENTEROcocci) Can occur as part of normal flora in the gut and can cause urinary, biliary, and cardiovascular infections. Resistant to Penicillin G and can GROW in 6.5% NaCl (while others canNOT)
Most commonly a nosocomial infection.

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Where do you find the different strains of Streptococci commonly on the body?

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S. Pneumoniae and Viridans found in oropharynx.
S. Pyogenes on Skin
S. Agalacticae in the female genital tract
S. Faecalis can occur in GI tract (enterococci remember?)

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Pathogenesis of Strep Family of Bacteria:

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Streptokinase a fibrinolysin can activate plasminogen
Hyaluronidase: hydrolyzes the ground substance of CT
Streptolysin (S - oxygen stable, toxic to tissue, RBC, Leukocytes, O oxygen labile and inactivated by oxidation - binds cholestrol , toxic to heart and other tissues)
M-protein anti phagocytic proteins
Erythrogenic toxin: superantigen responsible for scarlet fever rash (produced by S. Pyogenes)

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Clinical Findings of Streptococci?

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Most commonly S. pyogenes cause of strep throat--fever, sore throat, inflammation, pharyngitis, cellulities.
Strep Agalacticae: neonatal sepsis (group B) and meningitis
Strep Faecalis: Enterococci can cause urinary, biliary, cardiovascular
Viridans: oral microbiota (dental plaque), endocarditis

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Post streptococcol sequela?

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Immunological reactions to S. Pyogenes (due to M Protein, antibodies to different M proteins react to different host cells)
Rheumatic Fever: antibodies against certain M Proteins react with myosin protein in heart (heart valve damage) Can occur after any Group A infection (most typically after pharyngitis)

Acute Glomerulonephritis: M protein (most commonly 49) antigen antibody complex get lodged in glomerulus leading to Hypertension, edema of face and ankles, and smoky ankles. Most typically occurs after skin infection/pharyngitis.

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Important properties of Strep Pneumonia?

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Lancet shaped or spherical diplococci.
Polysaccharide capsules with antigenic distinction (quellung reaction used to distinguish).
Capsules are virulence factors that can interfere with phagocytosis (can combat with opsonization)
Opsonization occurs when body is able to produce the antibodies as a result of previous infection or a vaccine
Capsular Polysaccharide elicits B-cell response primarily.
Typically non transmissible.

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Pathogenesis of Strep Pneumoniae

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Capsule: ONLY encapsulated strains are virulent!!!!!
Secretory igA protease which destroys IgA antibodies
Pneumolysin (similar to Streptolysin O) makes pores in the cell membrane and activates inflammatory response.

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Streptolysin O

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Hemolysin Oxygen Labile (inactivated by oxidation): binds cholestrol and toxic to heart and other tissues. causes beta hemolysis

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Streptolysin S

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Oxygen Stable: Oxygen stable. Leukocidic, and kills RBCs and other tissues

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Clinical Findings of Pneumonia

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Chill, fever, cough, and pleuritic pain. red sputum formation with bacteremia in 15-25% of cases. Recovery can occur over time with anti capsular antibodies. **Risk for bacterial meningitis!