Cellulitis, by any other name.

“I know it when I see it . . . ,” as Justice Potter Stewart famously said of hard-core pornography. Would that this were the case with cellulitis. In principle, cellulitis is simply defined as an acute infection with inflammation of the skin involving the dermis and subcutaneous tissues. In practice, because of the overlapping signs and symptoms of skin infections, the terminology has become burdened with terms such as erysipelas, purulent cellulitis, nonpurulent cellulitis, nonsuppurative cellulitis, cellulitis with drainage, cellulitis with ulcer, cellulitis with abscess, abscess with surrounding cellulitis, and necrotizing cellulitis (to name a few), in an effort to parse differences in microbiology, severity, and prognosis that may impact therapy and management. At the semantic other extreme is International Classification of Diseases, Ninth Revision coding, which lumps cellulitis and abscess together, even though these 2 entities would appear to be easily differentiated clinically and microbiologically. Clearly, an abscess is a collection of pus often in association with pain, swelling, and inflammation. Whatever cellulitis is, it is not an abscess, as there is no collection of pus, which, if there were, the lesion would be an abscess and not cellulitis. Presence of a collection of pus affords the clinician great comfort, diagnostically and therapeutically. It is abscess defining, and culturing it permits a precise microbiological diagnosis. By far the most common cause of skin abscesses (barring unusual exposures or injury such as brackishwaterorbites) isStaphylococcusaureus, and pus and abscess formation are its modus operandi. Treatment is quite straightforward: Drain the pus, all of it. If an antimicrobial is needed (a topic that is well beyond the scope of this editorial), a narrowly defined microbiology allows for specific,pathogen-directedantimicrobial therapy against both methicillin-susceptible and methicillin-resistant strains of S. aureus. With respect to cellulitis, lack of clarity about the microbiology is a problem. If blood culture is the gold standard for microbiological diagnosis, then β-hemolytic streptococci cause the majority of cases of cellulitis (57%–75%) and S. aureus causes only 14% [1]. However, blood cultures are negative in ≥90% of cases [1–3]. In blood culture–negative cases, serological testing with anti-streptolysin O and anti-DNase-B indicates that β-hemolytic streptococci account for 70% of these infections [3]. If culture of the skin by various means, including punch biopsy, aspirate, or swab, is deemed the gold standard, then these proportions are essentially reversed. Staphylococcus aureus is isolated in 50%–82% of cases in which a culture is positive and β-hemolytic streptococci in only 9%–28% [4, 5]. If prevalent in the community, a substantial proportion of the S. aureus isolates are methicillin-resistant S. aureus (MRSA) [4, 6–8]. Pus, an ulcer, or other purulent drainage is invariably the material that has been cultured for cellulitis from which MRSA has been isolated [4, 6, 8]. As with blood cultures, cultures of skin specimens are usually negative and in the range of 72%–84% of all cellulitis cases [4, 5]. The study by Ells et al [9] of nasal colonization in patients with cellulitis and negative blood and skin cultures suggests that cellulitis is unlikely to be due to S. aureus. Staphylococcal colonization tracks very closely with concomitant infection and these investigators found that rates of colonization for cellulitis and uninfected controls were similar and neither was different from that expected for a general population [9]. Considering all of the available data, a skin infection with pus, either an abscess or purulent drainage, is strongly associated with isolation of by S. aureus, whereas infection without pus is not. In the latter instance, β-hemolytic streptococci are very likely the cause of the infection. Received 15 February 2013; accepted 19 February 2013; electronically published 1 March 2013. Correspondence: Henry F. Chambers, MD, Division of Infectious Diseases, San Francisco General Hospital, Bldg 30, Rm 3400, 1001 Potrero Ave, San Francisco, CA 94110 ([email protected]). Clinical Infectious Diseases 2013;56(12):1763–4 © The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: [email protected]. DOI: 10.1093/cid/cit126