With respect to cellulitis, lack of clarity about the microbiology is a problem. If blood culture is the gold standard for mi crobiological diagnosis, then β-hemolytic streptococci cause the majority of cases of cellulitis (57%-75%) and S. aureus causes only 14% [1]. However, blood cul tures are negative in >90% of cases [1-3]. In blood culture-negative cases, serologi cal testing with anti-streptolysin Ο 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 es sentially reversed. Staphylococcus aureus is isolated in 50%-82% of cases in which a culture is positive and β-hemolytic strep tococci in only 9%-28% [4, 5]. If preva lent 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 sug gests that cellulitis is unlikely to be due to S. aureus. Staphylococcal colonization tracks very closely with concomitant in fection 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 iso lation of by S. aureus, whereas infection without pus is not. In the latter instance, β-hemolytic streptococci ar