Management of Skin & Skin-Structure Infections in the Outpatient Clinic: An Update for Wound Care Providers

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.

References 

1. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of america. Clin Infect Dis. 2014;59(2):e10-52.

2. Swartz MN. Clinical practice. cellulitis. N Engl J Med. 2004;350(9):904-12.

3. Imadojemu S, Rosenbach M. Dermatologists must take an active role in the diagnosis of cellulitis. JAMA Dermatol. 2016; Nov 2. doi: 10.1001/jamadermatol.2016.4230. [Epub ahead of print.]

4. Strazzula L, Cotliar J, Fox LP, et al. Inpatient dermatology consultation aids diagnosis of cellulitis among hospitalized patients: a multi-institutional analysis. J Am Acad Dermatol. 2015;73(1):70-5.

5. Raff AB, Kroshinsky D. Cellulitis: a review. JAMA. 2016;316(3):325-37.

6. Schnyder B. Approach to the patient with drug allergy. Med Clin North Am. 2010;94(4):665-79.

7. Macy E, Ngor EW. Safely diagnosing clinically significant penicillin allergy using only penicilloyl-poly-lysine, penicillin, and oral amoxicillin. J Allergy Clin Immunol Pract. 2013;1(3):258-63.

8. Macy E, Contreras R. Health care use and serious infection prevalence associated with penicillin “allergy” in hospitalized patients: a cohort study. J Allergy Clin Immunol. 2014;133(3):790-6.

9. MacFadden DR, LaDelfa A, Leen J, et al. Impact of reported beta-lactam allergy on inpatient outcomes: a multicenter prospective cohort study. Clin Infect Dis. 2016;63(7):904-10.

10. Blumenthal KG, Shenoy ES, Wolfson AR, et al. Addressing inpatient beta-lactam allergies: a multihospital implementation. J Allergy Clin Immunol Pract. 2017;5(3):616-25.

11. Macy E, Contreras R. Adverse reactions associated with oral and parenteral use of cephalosporins: a retrospective population-based analysis. J Allergy Clin Immunol. 2015;135(3):745-52.

12. Dryden MS. Complicated skin and soft tissue infection. J Antimicrob Chemother. 2010;65(Suppl 3):35-44.

13. Stryjewski ME, Chambers HF. Skin and soft-tissue infections caused by community-acquired methicillin-resistant staphylococcus aureus. Clin Infect Dis. 2008;46(Suppl 5):S368-77.

14. Russo A, Concia E, Cristini F, et al. Current and future trends in antibiotic therapy of acute bacterial skin and skin-structure infections. Clin Microbiol Infect. 2016;22(Suppl 2):S27-36.

15. Peterson LR, Quick JN, Jensen B, et al. Emergence of ciprofloxacin resistance in nosocomial methicillin-resistant staphylococcus aureus isolates. resistance during ciprofloxacin plus rifampin therapy for methicillin-resistant s aureus colonization. Arch Intern Med. 1990;150(10):2151-5.

16. Blumberg HM, Rimland D, Carroll DJ, Terry P, Wachsmuth IK. Rapid development of ciprofloxacin resistance in methicillin-susceptible and -resistant staphylococcus aureus. J Infect Dis. 1991;163(6):1279-85.

17. Hooper DC. Emerging mechanisms of fluoroquinolone resistance. Emerg Infect Dis. 2001;7(2):337-41.

18. Griffiths CL, Gutierrez KC, Pitt RD, Lovell RD. Eosinophilic pneumonia induced by ceftaroline. Am J Health Syst Pharm. 2014;71(5):403-6.

19. Furtek KJ, Kubiak DW, Barra M, et al. High incidence of neutropenia in patients with prolonged ceftaroline exposure. J Antimicrob Chemother. 2016;71(7):2010-3.