Cellulitis is a diffuse bacterial skin infection with an incidence rate of around 200/100 000/year. Erysipelas is the superficial variant characterized by sharply demarcated erythema. Streptococcus pyogenes (GAS) and other β-hemolytic streptococci are the main causes of erysipelas. However, in deeper forms of cellulitis, the etiology has been more unclear. Previous studies using culture of biopsies have suggested a major role for Staphylococcus aureus, but recent molecular studies and clinical trials indicate that S. aureus found in cellulitis might often represent colonization.
We have combined serology, culture, and penicillin response data in prospective studies comprising 230 adult patients hospitalized with erysipelas or deeper cellulitis. Evidence of a streptococcal origin was found in more than 80% of the cases, including the majority of patients without typical signs of erysipelas and those with facial location, purulence, or comorbidities such as diabetes mellitus. β-hemolytic group C or G streptococci (GCS/GGS) were more commonly isolated than GAS. GCS/GGS infections were primarily located in the lower extremities and were associated with a rise in anti-streptolysin-O just as often as GAS. Most cases with S. aureus cultured from swabs had serological evidence of streptococcal infection. Together, the findings suggest that cellulitis essentially is a streptococcal disease.
Cardiovascular disease and overweight were associated with delayed treatment response, illustrating the importance of host factors in the course of streptococcal disease. We also frequently observed inflammation that increased during treatment and inflammation that persisted after treatment, reflecting the ambiguous relationship between infection and inflammation and possibly variable pathogen toxicity.
Cellulitis displays the importance and variability of host and pathogen factors in streptococcal disease.