Properties

Pathogenesis

Clinical findings

Laboratory diagnosis

Treatment & Prevention

Staphylococci aureus

Gram positive cocci

Irregular grapelike clusters.

Catalase positive.

Nonmotile.

Do not form spores.

Forms golden yellow colonies.

Not regarded as part of normal flora but is carried by a large proportion of population at any one time.

Commonest carriage site is the skin at the front of the nasal cavity.

Virulence factors:

- protein A binds Fc portion of IgG molecule, inhibiting opsonization.

- teichoic acids mediate adherence of staphylococci to mucosal cells.

- surface receptors for specific staphylococcal bacteriophage.

Cause diseases by:

- producing toxins

- multiplying in tissue, causing inflammation.

Typical lesion is an abscess which undergo central necrosis & usually drain to the outside (e.g. furuncles & boils).

Toxins:

- enterotoxin causes vomiting & water & nonbloody diarrhea; acts by stimulating large amounts of IL-1 & IL-2; heat-resistant.

- toxic shock syndrome toxin: a superantigen which causes toxic shock by stimulating the release of large amounts of IL-1 & IL-2.

- exfoliatin causes ‘scalded-skin’ syndrome in young children; also a superantigen.

- alpha toxin causes marked necrosis of skin, hemolysis & destroy phagocytes.

Enzymes:

- coagulase

- fibrinolysin

- hyaluronidase

- proteases

- nucleases

- lipases

Inflammatory:

- skin infections: impetigo (superficial skin), furuncles (hair follicle/sebaceous gland), carbuncles (multiple sites), cellulitis (subcutaneous tissue), surgical wound infections, eyelid infections & postpartum breast infections.

- bacteremia, can lead to abscesses anywhere, including in the kidney, brain & lung.

- endocarditis on normal or prosthetic heart valves.

- osteomyelitis & septic arthritis.

- pneumonia in postoperative patients or following viral respiratory infection.

Toxin-mediated:

- enterotoxins A-E: food poisoning due to ingestion of heat-stable enterotoxin; vomiting, prostration, diarrhea.

- toxic shock syndrome: acute illness with fever, a diffuse erythematous rash, hypotension.

- scalded skin syndrome: superficial layers of the epidermis slough in response to exfoliatin (epidermolytic toxins A & B); intra-epidermal blisters at site of infection – pemphigus neonatorum.

Gram stain: typical Gram positive cocci.

Culture:

- golden yellow colonies.

- usually beta-hemolytic.

Treatment:

- drainage of pus.

- removal of any foreign material.

Antibiotics:

- produce beta-lactamase enzyme which destroy penicillin.

- naficillin

- erythromycin

- cephalosporins.

Methicillin-resistant S.aureus (MRSA):

- will not respond to any penicillin or cephalosporin.

- have to use vancomycin.

Prevention:

- cleanliness, frequent handwashing, aseptic management of lesions help prevent spread of S.aureus.

- dissemination from nose or skin of carriers can be reduced by topical application of antimicrobial agents.

- remove shedders from high-risk areas, e.g. operating theatres, nurseries.

Staphylococcus epidermidis

Coagulase-negative.

Forms white colonies

Sensitive to novobiocin

Part of normal human flora on the skin and mucous membranes.

Produces large amounts of slime which allow them to adhere to the surface of any material introduced into the body.

Cause infections of intravenous catheters & prosthetic implants, e.g. heart valves.

Major cause of sepsis in neonates.

Vancomycin + rifampin or an aminoglycoside.

Staphylococcus saprophyticus

Coagulase-negative.

Forms white colonies.

Insensitive to novobiocin.

Common cause of urinary tract infection, particularly in sexually active young woman.

Second to E.coli as a cause of community-acquired urinary tract infections.

Norfloxacin.

Trimethoprim-sulfamethoxazole