place or within one year in the presence of an implant and the infection appears to be related
to the surgery.
Pathogenesis of SSI varies with the type of surgical procedure. Implicated pathogen is
usually the patient’s endogenous flora of patient’s skin, mucous membranes, or hollow viscera.
Gram-positive cocci (S. aureus, coagulase-negative staphylococci) from the patients skin flora
or exogenous environment is the usual pathogen following clean surgical procedure but may
include anaerobes and gram-negative when incisions are made around the groin or perineum.
Polymicrobial infections are often seen in clean-contaminated, contaminated or dirty wounds.
Acute onset within 24 to 48 hours postoperatively or after trauma with systemic manifestation
are usually due toStreptococcusandClostridiumsp. TSS due toS. aureuscan occur in rare
instances. Fever, hypotension, abnormality in renal, and liver function can occur. The primary
treatment for most SSI is to open the incision and evacuate the infected material. Antibiotic
therapy can be guided by findings of Gram stain and wound cultures (13,39).
SYSTEMIC SYNDROMES
Staphylococcal Scalded Skin Syndrome
SSSS, first described in 1956, is a generic term applied to a group of exfoliative dermopathies
caused by an exfoliative (or epidermolytic) exotoxin, produced by various strains ofS. aureus;
mainly of phage group II (usually type 71) (82–84). It primarily affects neonates and young
children; although adults with underlying diseases are also susceptible. Two variants of the
toxin, the exfoliative toxin A and B have been described. These exotoxins induce pathological
changes in the epidermis that closely resemble a scald caused by boiling water, hence the name
SSSS (85–87). Histologically, these toxins cause intraepidermal cleavage through the granular
layer without damage or alteration of the keratinocytes, bullae formation; and slippage of
the upper epidermal layer with the application of gentle pressure (a positive Nikolsky sign).
S. aureusenterotoxin (A through D) and toxic shock syndrome toxin 1 (TSST-1) are frequently
associated with staphylococcal scarlet fever. The clinical response to these exotoxins is varied.
Thus, the manifestations of SSSS include several primarily age-dependent presentations: (i)a
generalized exfoliative syndrome seen in newborns (Ritter’s disease or Pemphigus neo-
natorum) and children, but can rarely develop in adults; (ii) bullous impetigo, a localized
pustulosis in children; and (iii) staphylococcal scarlet fever, form of SSSS that does not progress
beyond the initial stage of a generalized erythematous eruption.
SSSS occurs abruptly or few days after a recognized staphylococcal infection with fever,
skin tenderness, and scarlatiniform rash. The lesions begin as a vesicle that gradually
enlarges into flaccid bullae that rupture, leaving a tender, moist surface that eventually heals.
Localized infection occurs usually in the nasopharynx, umbilicus, or urinary tract. Large
flaccid clear bullae form over two to three days and result in separation of sheets of skin.
Exfoliation exposes large area of bright red skin surface (88,89). Fluid and electrolyte loss can
lead to hypovolemia and sepsis syndrome. In adults the mortality rate approaches 60% (90).
With appropriate therapy the lesions heal within two weeks. Toxic epidermal necrolysis
(TEN) typically occurs as a drug reaction. The lesions are similar to SSSS, however it has
more extensive destruction of the epidermis and the stratum corneum layer, recovery is
prolonged, and scarring is more frequent. TEN is often fatal and should be treated like a
widespread burn. Most cases of SSSS are diagnosed on clinical grounds and are easily treated
with antibiotics, which rapidly eliminate thestaphylococci producing the toxin. Laboratory
investigations are required only if the clinical findings are equivocal or when outbreaks
occur. Because the condition is the result of exotoxins that may be produced by staphylococci
at a distant site, the blister fluid in generalized SSSS tends to be sterile, whereas the fluid in
localized bullous impetigo will containS. aureus. Staphylococci producing ET can usually be
cultured from the nares, conjunctiva, or nasopharynx. Biopsy of the blister is one of the most
definitive diagnostic tests in SSSS. One study revealed a positive blister biopsy result with
intraepidermal cleavage in all 30 adults with SSSS (89). Blood cultures are usually negative
because the organisms are frequently noninvasive, particularly in children. In one study,
only 3% of children had a positive blood culture, in contrast to 20 (62.5%) of 32 adults
(86,89,91–93).
Severe Skin and Soft Tissue Infections in Critical Care 311