Skin and skin-structure infections (SSSIs) result in significant morbidity in both the community and hospital settings.1 Most often, SSSIs are caused by Gram-positive bacteria, such as Staphylococcus aureus, Streptococcus pyogenes, and other β-hemolytic streptococci. Detection of pus, or lack thereof, can further assist the clinician in identifying the likely pathogen. A purulent SSSI suggests S. aureus involvement, whereas a nonpurulent SSSI is often caused by Streptococcus sp. Alternatively, Gram-negative organisms may cause SSSIs in the perianal region or lower abdomen, infectious gangrene, or superinfection of preexisting lesions. Diagnosis of SSSIs is primarily based on physical and clinical findings. Importantly, noninfectious processes (eg, deep venous thrombosis, Sweet’s syndrome, gout) may mimic SSSIs and, therefore, must be excluded, as misdiagnosis rates may reach 30%.2-4 Superficial wound cultures, particularly from chronic wounds or ulcers, are frequently polymicrobial with a plethora of organisms. Frequently, the resultant bacterial growth represents colonization, proliferating organisms that do not elicit a host response, and can even include multidrug-resistant pathogens, rather than the underlying etiology.5 If indicated, deep tissue cultures following cleansing and debridement provide the most reliable information about the infectious etiology.
Some SSSIs, such as simple abscesses or boils with accompanying erythema < 5 cm, do not require antibiotics because incision and drainage alone is sufficient.1,2 Antibiotic selection has become more challenging due to increasing rates of resistance in combination with patient-specific factors, including comorbidities and allergies. While broad-spectrum therapy for all patients may seem to solve this dilemma, it is unnecessary and should not be routinely used because many narrower spectrum antibiotics will successfully eradicate the associated pathogens. Importantly, allergic reactions should be explored and documented judiciously (see Table 1).6 Approximately 10% of the United States population reports penicillin allergies, however, < 1% are truly allergic.7 Avoidance of β-lactams (eg, penicillins, cephalosporins) due to reported allergy decreased the use of preferred therapies while increasing the rate of unwanted outcomes, including Clostridioides difficile-associated diarrhea, higher incidence of methicillin-resistant S. aureus (MRSA) and vancomycin-resistant enterococci, and adverse events.8,9 Skin testing for penicillin allergy may assist in correctly identifying patients who are not truly allergic and allow for the receipt of safer or less toxic antibiotics.10 Furthermore, cross-reactivity between penicillins and cephalosporins is becoming less of a concern, as almost all patients who live with penicillin allergy can receive cephalosporins without incident.11
Empirical antibiotics for SSSIs should primarily target S. aureus and S. pyogenes with additional coverage depending on risk factors (see Table 2 ).1,5,12-14 However, if available, antibiotic selection should be based on microbiologic data in addition to clinical presentation and the aforementioned factors. While some new antibiotics have been released, oftentimes older antibiotics will produce the same outcome (see Table 3).1,5,14-19 Additionally, clinicians must recognize that in vitro susceptibility provided by the microbiology laboratory does not always equate to in vivo efficacy in their patients. Appropriate use of antibiotics for the shortest duration necessary can improve patient outcomes while minimizing the contribution to the ongoing threat of antibiotic resistance.
Daniel B. Chastain is clinical assistant professor at the University of Georgia College of Pharmacy, Albany, and the infectious diseases pharmacy specialist at Phoebe Putney Memorial Hospital, Albany. Gregory M. Steele is a nurse practitioner the infectious diseases department at Phoebe Putney Memorial Hospital.
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