A variety of terms describing infections of the skin and underlying soft tissue structures are used, including terms used by the Food and Drug Administration (FDA) and oth­ers used more commonly in clinical practice. For the pur­pose of therapeutic clinical trials (predominately antibiotic

2. Necrotizing SSTIs (NSSTIs): (a) Necrotizing cellulitis (b) Necrotizing fasciitis (c) Necrotizing myositis and myonecrosis

3. Incisional surgical site infections: (a) Superfi cial (b) Deep

3 , 8 ]. NSSTIs may

also be classifi ed by the bacterial pathogenesis of the infec­tion as [

The deep fascia is much more susceptible to infection than either the dermal or muscular tissues and is thus more frequently involved in necrotizing infectious processes. The deep fascia has tenuous blood supply, and its attachments to adjacent tissues are easily disrupted, creating an avascular compartment that allows the collection of fl uid and the rela­tively uninhibited spread of infection along the fascial plain. The tenuous nature of fascia explains its susceptibility to necrotizing infection and why fasciitis is more common than necrotizing cellulitis and myositis, accounting for greater than 70 % of necrotizing infections.

Bacterial reproduction rate is also a signifi cant determinate of the patients clinical course and presentation. Bacterial reproduction determines the rate at which the number of bacteria will increase within the host tissue. Thus, species that rapidly reproduce and have signifi cant toxin production that enhances virulence can invade normally resistant tissues and initiate a rapidly progressive infection, either as a single patho­gen or in concert with other pathogens. GAS, community­associated methicillin-resistant S. aureus (CA-MRSA), and clostridial species are the commonly encountered pathogens that may produce rapidly progressive soft tissue infections, although a variety of other pathogens may do so including Vibrio , Aeromonas , Eikenella , Pasteurella , and Bacillus species [

The dramatic rise in the incidence of CA-MRSA-related SSTI over the past several decades justifi es expanded discus­sion. In the early 1980s, community outbreaks of MRSA SSTI infections began to be reported in patients without standard risk factors for MRSA [ noted to have antibiotic sensitivities that were not typical of hospital-associated MRSA, and thus the term community­associated was applied to the organisms. Outbreaks were reported in otherwise healthy Alaskan natives, children, inmates in correctional facilities, institutionalized adults with developmental disabilities, nursing homes, and athletes [ 6 ]. Over the subsequent decades, the incidence of CA-MRSA has increased, and in most locations it is the most common skin and soft tissue infection pathogen [ 14 – 16 , 21 – 23 ].

Discussion will focus on those infections that are pertinent to decisions in surgical or critical care settings including non­necrotizing cellulitis, bite wounds, and complex abscesses.

41 , 42 ]. However, treatment failures with beta-lactam antibi- otics do occur despite in vitro microbial sensitivity to the agents used [ 43 – 46 ]. The mechanism of failure is believed to involve the failure of bacterial killing by cell wall-inhibiting agents when high numbers of bacteria in the static phase lead to decreased expression of penicillin-binding proteins [ 46 – 48 ]. Protein synthesis inhibitory agents such as macrolide and lincosamide antibiotics may be as effective and potentially superior in certain settings [ 45 , 46 , 49 ]. Clindamycin either alone or in combination with a cell wall-inhibiting agent was found to be more effective than cell wall- inhibiting agents alone in a retrospective analysis of pediatric group A strepto­coccal infection [ 46 , 49 ]. Roxithromycin proved to be equiv- alent to penicillin for the treatment of erysipelas in a randomized, multicenter trial [ 50 ]. However, increasing macrolide resistance among streptococci introduces concern for these agents, and local sensitivity patterns should be con­sidered when using these agents alone for the treatment of complicated group A streptococcal infections [ 46 , 51 , 52 ]. Additionally, since clindamycin has been demonstrated to reduce exotoxin and superantigen production by pathogenic strains of group A streptococci, the drug is frequently used as an adjunct in the treatment of streptococcal toxic shock syn­drome [ 45 , 48 , 53 ]. However, the most effective antibiotic regimen in this setting has not been established in prospec­tive studies. If methicillin-sensitive S. aureus is suspected, the treatment of choice is a penicillinase-resistant semisyn­thetic penicillin or a fi rst-generation cephalosporin for non­methicillin- resistant staphylococcal infections [ 3 , 25 ]. However, as previously discussed, the recent dramatic increase in community-associated MRSA makes the empiric treatment of staphylococcal infections with beta-lactam anti­biotics problematic, and other agents should be considered unless the risk of resistant staphylococcus is low (see discus­sion below) [

55 , 56 ]. Infection rates vary widely depend-

ing on the severity of the bite wound, the location of the bite wound, and the animal source. Nonhuman bites that are low risk and not involving the hand have infection rates that appear to be less than 2 %; human bites involving the hand with signifi cant penetration have infection rates of greater than 50 %. Unfortunately very limited data exists to guide the principle management of bite wounds including (1) irriga­tion, debridement, or decontamination of the wound, (2) pri­mary wound closure, (3) prophylactic antibiotics, and (4) therapeutic antibiotics. Thus, most recommendations are based on consensus opinion and not randomized data.

56 , 57 ]. A