NAME OF DISEASE: Furunculosis - focal suppurative inflammation of the skin and
Folliculitis - hair follicle infection
Hidradenitis - sweat gland infection
Carbunculosis - a deep infection producing multiple, adjacent draining
Scalded skin syndrome
ETIOLOGICAL AGENT: Staphylococcus aureus
Although there are a number of antigens on the surface of the staphylococcal cells, it is difficult to serologically type the cells. Instead phage typing is used. These are the hardiest of the non-sporeforming bacteria.
Most adults are continuously exposed to S. aureus but overt infection occurs in 1 of 20 people each year. Predisposing factors include:
1. Hypogammaglobulinemia - congenital or acquired
2. Diabetes mellitus - high
concentration of ketone bodies inhibits the intraleukocytic killing of
engulfed S. aureus.
3. Chronic Granulomatous
Disease - Neutrophils cannot make sufficient H2O2
to set off the
Pathology is the result of:
1. Toxin production
Exfoliative toxin (plasmid-borne and in 5% of S. aureus)
Toxic shock toxin
2. Hemolysin production
a- dermonecrotic, causes aggregation of platelets and spasms of smooth muscle
ß - sphingomyelinase
d- detergent-like activity
g- weaker and not well characterized
3. Enzyme production
4. Envelope component production
Murein - activates complement
Teichoic acid - activates complement, functions in adherence
Protein A - binds Fc terminus of IgG
The clinical manifestations of the skin may vary from a small pimple to a large furuncle or carbuncle (a deeply situated infection producing multiple adjacent draining skin sinuses) with rapid destruction of skin. Definitive diagnosis is by isolation of the organism from the site of infection or by demonstration of antibodies against staphylococcal teichoic acid antigens via simple agar gel diffusion or counterimmunoelectrophoresis (CIE). The hallmark of the disease is pus formation.
Treat with penicillinase - resistant penicillins such as:
If the organism is methicillin-resistant treat with:
Drain the wound via surgical incision.