see also:

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

• 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);
• Some produce:
  • enterotoxin (heat stable; in food poisoning);
  • 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;
  • 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 ¹⁾
• 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 ²⁾
• 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