Medsci 202 - Staphylococcus Aureus

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Characteristics of Staphylococci

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→ Gram positive
→ spherical cells (cocci); found in irregular 'grape-like' clusters
→ non motile (no flagella)
→ sometimes pigmented (aureus = gold)
→ resistant to dry conditions = up to 10% NaCl (halodurent) = due to capsule

Front 2

Epidemiology of Staphylococci

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→ opportunistic pathogens = colonizing moist skin folds, oropharynx, gastrointestinal tract and urogenital tract
→ ~15% are carriers of S. aureus (in the nose)
→ transmission = human to human (shedding)
→ prevalent amongst hospital staffs = hospital-acquired infections

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Drug Resistance of Staphylococci

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→ >90% are resistant to penicillin = carry β-lactamase gene
→ 'super bug' = methicillin-resistant strains (MRSA) and vancomycin-resistant strains
→ Hospital-acquired MRSA (1960s)
→ Community-acquired MRSA (1990s)

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Diagnosis of Staphylococci

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1. gram-positive cocci
2. catalase test → +ve
3. coagulase test → +ve = only S. aureus can coagulate fibrinogen
3. mannitol salt agar → S. aureus = yellow ferment

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What are Virulence Factors?

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→ gene products that enable a bacteria to colonise, damage and infect a host tissue while evading immune responses

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Adhesins (Virulence Factor)

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→ microbial surface components recognizing adhesive matrix molecules (MSCRAMMS)
→ cell wall attached proteins in gram positive bacteria
→ allow bacteria to bind to ECM proteins of host cell = fibronectin, elastin, laminin, vitronectin and collagen
→ important for tissue colonisation

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Cytolysins (Virulence Factors - Host Cell Damage)

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→ cell damaging proteins
→ alpha (α) toxin = produces a heptameric pore into membrane causing leakage + osmotic imbalance hence haemolysis
→ beta (β) toxin = sphingomyelinase C = hydrolyzes membrane sphingomyelins
→ delta toxin = surfactant detergent actions (amphipathic)
→ gamma (γ) toxin + Panton-Valentine leukocidin (PVL) = pore forming proteins

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What cells do Cytolysins damage?

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→ they are toxic for many cells
1. leukocytes = immune evasions
2. erythrocytes = access to iron (Heme and lactoferen)
3. tissue cells = bacterial spreading

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Exfoliative Toxins (Virulence Factors - Host Cell Damage)

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→ serine proteases that split intercellular bridges (desmosomes) in stratum granulosum
→ results in skin peeling
→ no cytolysis or inflammation
→ produced by 5-10% of S. aureus strains

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Spreading Factors

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→ proteins (enzymes) that facilitate spreading of localized infection to surrounding tissue or blood (bacteremia)

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Type of Spreading Factors

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1. Lipases - hydrolyses lipids = invasion of cutaneous tissues
2. Nucleases - hydrolyses DNA = decrease viscosity of pus
3. Hyalurodinase - hydrolyses hyaluronic acid in connective tissue
4. Proteases - serine proteases + aureolysin
5. Staphylokinase (fibrinolysin) - causes fibrinolysis (dissolves clots)

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Immunopathogenic Factors (Superantigens)

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→ Toxic Shock Syndrome Toxin (TSST) + Staphylococcal Enterotoxins (SEA, SEB)
→ TSST = stimulates T cells which release pro-inflammatory cytokines (TNF-α) and IFN-γ = systemic inflammation
→ also cause food poisoning

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Capsule (Immune Evasion Factors)

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→ dense polysaccharide coat = prevents opsonisation from antibodies + compliments (prevents phagocytosis)
→ contains water = prevents dessication

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Slime Layer (Immune Evasion Factors)

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→ loose bound water soluble (biofilm)
→ made from secreted polysaccharides
→ protects from immune factors + antibiotics

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Catalase (Immune Evasion Factors)

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→ detoxifies peroxides (prevents killing mechanism of macrophages and neutrophils)
→ used to distinguish Staphylococcus (produces oxygen - bubbles) from Streptococcus

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Clumping Factor CIF-A (Immune Evasion Factors)

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→ binds fibrinogen, converts to insoluble fibrin
→ fibrin production = prevents opsonisation + phagocytosis
→ promotes cell aggregation (clumping)
→ coagulase test = identifies S. aureus
→ fibrin also allows undetectability from leukocytes

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Protein A (Immune Evasion Factors)

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→ found on most S. aureus strains = binds to IgG (except IgG3) in "wrong orientation" via Fc region
→ prevents opsonisation + phagocytosis

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Impetigo (Superficial S. aureus skin Disease)

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→ localised in cutaneous infections = pus filled vesicles
→ eventually dries out = crust
→ primarily affects young children

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Folliculitis (Superficial S. aureus skin Disease)

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→ impetigo involving hair follicles

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Furuncles/Boils (Superficial S. aureus skin Disease)

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→ painful pus filled cutaneous nodules

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Carbuncles (Superficial S. aureus skin Disease)

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→ coalescence of furnucles = extension into subcutaneous tissue
→ can lead to bacteremia (bacteria in blood)

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Corneal Ulcer (Superficial S. aureus eye Disease)

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→ deep infection of the cornea = after abrasion (contact lenses)

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Bacteremia (Invasive Disease)

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→ spread of bacteria in the blood = organ infection (endocarditis)

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Endocarditis (Invasive Disease)

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→ damage to the endothelial lining (outer layer) of the heart = infected heart valves has bacteria, platelets and cellular debris
→ S. aureus endocarditis = ~50% mortality rate
→ heart valve perforations via secreted enzymes
→ septic embolism

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Osteomyelitis (Invasive Disease)

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→ spread of blood (hematogenous dissemination) to bone or by secondary infection via trauma
→ infection of metaphyseal (tip) of long bone
→ cure rate = good with antibiotics

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Septic Arthritis (Invasive Disease)

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→ mainly from intra-articular injections or via hematogenous spread
→ painful erythematous (reddened) joint and purulent (pus filled) joint space

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Pneumonia (Invasive Disease)

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→ occurs after aspiration of oral secretion = hematogenous spread
→ abscess formation in lung via cytolytic toxins
→ necrotizing pneumonia = severe

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Staphylococcus Scaled Skin Syndrome - SSSS (Toxigenic Disease)

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→ caused by exfoliative toxins = desquamation (skin peeling) of epithelium (Ritter's Disease)
→ affects mostly neonatal + young children
→ low mortality rate; immunogenic

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Staphylococcal Food Poisoning (Toxigenic Disease)

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→ contamination of food via human carrier + improper food handling
→ microbial intoxication (not infection) = caused by heat stable enterotoxins (SEA, SEB)
→ severe vomiting, diarrhoea, abdominal pain, nausea sweating, headache

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Toxic Shock Syndrome - TSS (Toxigenic Disease)

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1. Menstrual TSS - growth of TSST strain in vagina (can penetrate mucosal barrier) → caused by prolonged use of tampon
2. Non-Menstrual TSS - growth of TSST in wounds → hematogenous spread of toxins causes systemic diseases = fever, hypotension, erythematous rash, multiple organ failure (30-40% mortality rate)

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Risk Factors of S. aureus

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→ presence of foreign body, poor hygience, hospital infections, inhibition of microflora via antibiotics, lack of antibodies

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Susceptible Patients

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→ infants (SSSS), poor hygiene (impetigo, boils)
→ menstruating women (TSS)
→ patients with intravascular catheter (bacteremia, endocarditis)
→ compromised pulmonary function (pneumonia)