see also:

• clinically important bacteria
• antibiotics for Rx of Staph. aureus
• innate immunity

• Gram +ve, spherical, often in clusters, non-motile, non-sporing;
• Catalase +ve; fermentative (cf. micrococcus oxidative);
• Some have capsules; aerobic & facultative anaerobes;
• Grow easily on most media, best at 37°C;
• Usually cream-yellow on blood agar within 24hrs; usually odourless;

• coagulase +ve (converts fibrinogen→fibrin coats bacteria);
• DNAase +ve; reside mainly in ant. nares (40-80% adults);
• can grow between about 7–48 °C, with enterotoxin production mainly between 10–48 °C and optimal around 40–45 °C
• Some produce:
  • enterotoxin (heat stable; in food poisoning);
    • toxin levels that cause illness usually require S. aureus populations above about 10⁵ CFU/g in the food
    • this toxin general causes a sudden onset of vomiting within a few hours of consuming the food and this vomiting generally lasts 4-5 hours - diarrhoea is not a feature.
    • at typical fridge temperatures (≤ 4 °C), S. aureus growth is effectively halted or becomes extremely slow, and enterotoxin production does not occur at these temperatures, nevertheless most would recommend sliced meats such as ham is consumed within 3-5 days when kept in a fridge and there has not been a “abuse period”
    • risk of enterotoxin food poisoning increases sharply if slices sit at room temperature (or warmer, e.g. buffet, car, esky at ambient) for several hours, especially if there is hand contact from a colonised handler, then are returned to the fridge; that abuse period is when toxin is formed and, once formed, the toxin is not destroyed by reheating or by refrigeration.
    • outbreaks are mostly linked to preparation and holding at unsafe temperatures in restaurants, delis or homes (food left in the danger zone), rather than to correctly refrigerated leftovers
  • alpha-toxin (hemolysin & leucocidin);
  • Panton-Valentine leucocidin;
  • exfoliatin (group II only);
  • toxic-shock toxin (group I only1);
  • penicillinase (group III);
  • eryhthrogenic toxin (→scarlet fever-like rash);
  • staphylokinase (lyses fibrin via activ. plasmin);
  • hyaluronidase;
• Grouped by phage typing into 3 main groups:
  • I - incl. many endemic hosp. strains;
  • II - incl. many cause minor sepsis/impetigo/exfoliatin;
  • III - incl. most enterotoxin strains & antib.res.strains;
• Lesions:
  • impetigo - pustule beneath stratum corneum epidermis;
    • Staph can strongly bind to cutaneous desmoglein-1 via serine-aspartate repeat protein D (SdrD) augmented by skin calcium levels (which are often higher in those with atopic dermatitis) and this bond is stronger than any other protein bond known in biology¹⁾
    • the outermost layer of skin, the stratum corneum (SC), consists of corneocytes which are connected by corneodesmosomes, primarily composed of desmoglein-1 (DSG-1), corneodesmosin (CDSN), and desmocollin-1; DSG-1 is expressed on the surface of both corneocytes and keratinocytes; S. aureus exfoliative toxins cleave the homophilic interaction site of DSG-1, causing cell detachment and compromising the SC barrier function. Mutations in DSG-1 are linked to dermatitis, multiple allergies, and metabolic wasting;
  • superficial folliculitis - superficial part hair follicle only;
  • boil (furuncle) - entire hair follicle → s/c;
  • carbuncle - pockets in s/c tissue due to fibrous septae, with communication b/n boils;
  • abscesses of pulp spaces/palmar spaces/etc.
  • mastitis from newborn via cracked nipples;
  • pneumonia
  • pseudomembranous enterocolitis;
  • osteomyelitis if bacteraemia + trauma or compound #;
  • renal carbuncle due to bacteraemia;
  • lymphadenitis;
  • septicaemia/pyaemia;
• in over 80% of cases of S. aureus bacteraemia, the Staph strain can be detected in the anterior nares of the patient which is presumably the site of endogenous colonisation ²⁾
• a third of the population carry St. aureus in their nose or on their skin
• whilst mainly extra-cellular, it has a capacity to adopt an intracellular behaviour, readily adhering to and invading various eukaryotic cells, including non-professional phagocytes
  • clinical mutations in ausA, encoding the aureusimine non-ribosomal peptide synthetase, reduces S. aureus cytotoxicity, and increases intracellular persistence ³⁾
• potent pore-forming toxins (PFTs), including alpha-hemolysin and leukocidins, are among the major virulence determinants of S. aureus and induce rapid host cell death, including death of the leukocytes and neutrophils recruited to remove bacteria from infected tissues

• (coagulase -ve) grouped via:
  • Novobiocin sens. → S.epidermidis
  • Novobiocin resist. → S.saprophyticus