Makindo Medical Notes.com

About

• Common skin commensal but significant pathogenicity
• Some of the released toxins are superantigens

Growth of Staph. aureus in blood cultures should never be dismissed as a ‘contaminant’ unless all possible underlying causes have been excluded and repeat cultures are negative. Could it be endocarditis

Characteristics

• Aerobes or facultative anaerobes and Salt tolerant
• Gram positive grape-like clusters. Coagulase-positive (forms a fibrin clot)
• Catalase positive and Beta haemolytic
• Protein A on surface binds Fc of IgG which reduces opsonisation and phagocytosis

Important causes of pathogenicity

• Coagulase positive - coagulates plasma
• Staphylokinase, Hyaluronidase, Enterotoxins
• Haemolysin - breaks down red blood cells
• Panton Valentine leucocidin - damages white blood cells
• Toxic shock syndrome toxin (TSST) - superantigens
• Exfoliative and epidermolysis toxins, Proteases
• Polysaccharide capsule - blocks phagocytosis
• Protein A - a surface protein that binds Fc portion of Ig blocking complement

Source

• Nasal mucosa, skin and vagina and groin and perineum
• Health care workers, IV drug users
• Diabetics and neutropenic

Pathogenicity

• Food poisoning: Heat stable enterotoxin in poorly refrigerated protein foods (eg canned or salted meat). Enterotoxins bind vagal nerve endings and cause nausea, abdominal pain and vomiting within 1-6 hours
• Skin: Bullous impetigo, eczema, folliculitis, furuncles, Carbuncles, Boils, mastitis, wound infections, cellulitis. Can release toxins causing exfoliation and scalded skin syndrome. Wound and cannula-related infections caused by Staph. aureus are seen in patients.
• Toxic epidermal necrolysis (Ritter-Lyell's disease)
• Toxic shock syndrome: surgical packing or highly absorbent tampons have been associated with Staph aureus growth and production of TSST-1 a superantigen (PTSag) which binds major histocompatibility complex II and causes T cell activation and a cytokine storm with massive cytokine release. Onset can be rapid and deterioration rapid especially in young otherwise well patients.
• Infective Endocarditis: Staph aureus binds readily to fibrinogen on normal heart endocardium. Fibronectin binding protein enhances adhesion. Local damage is caused by the production of alpha-toxin which is a pore-forming cytolysin. Typically, findings of endocarditis follow.
• Osteomyelitis, Pneumonia - in immunocompromised or post influenza with cavitation

Investigations

• Coagulase positive, DNAase production
• Detection of antibodies to Protein A and haemolysin
• Grows on Mannitol salt medium. Tolerates 5-10% NaCl
• Grows on blood agar to forms golden colonies at 37° aerobically and less well anaerobically
• Phage typing

Management

• MSSA
  • Penicillin resistant most strains produce beta-lactamases
  • Cephalosporins, Flucloxacillin, Fusidic acid, Vancomycin
  • Others are glycopeptides, Linezolid, Erythromycin and other Macrolides
• MRSA
  • Methicillin resistance is due to a modified chromosomal Penicillin-binding protein. Also have plasmid-mediated immunity to all other drugs except Vancomycin. Drug resistance transferred by phage
  • Use Vancomycin or Teicoplanin

Sensitivity