Abstract

Necrotizing fasciitis is perhaps the most severe form of soft tissue infection primarily involving the superficial fascia and subcutaneous tissue. This condition is associated with severe sepsis, a fulminant course and high mortality. While group A Streptococcus (GAS) remains the most common etiologic agent in necrotizing fasciitis due to a single organism [1], we have recently noted an emergence of group B Streptococcus (GBS) or Streptococcus agalactiae as a causative agent. This report describes our recent experience with GBS necrotizing fasciitis seen in Singapore between the years 2000 and 2002. Five patients with monomicrobial necrotizing fasciitis caused by GBS were identified during this time period. All patients were female, with ages ranging from 38 to 66 years. Diabetes mellitus was a frequent association and was noted in four of the patients. Early aggressive surgical debridement is the cornerstone management of necrotizing fasciitis and was performed in all cases. The procedure was repeated until all necrotic and non-viable tissues were excised. Two to three debridements were necessary to achieve this. The group B streptococci isolated from all five patients were susceptible to penicillin, ampicillin and erythromycin. Table 1 summarizes the clinical presentation, antimicrobial therapy and outcome of the five cases. At our hospital, we generally treat patients with severe GBS soft tissue infections with high-dose parenteral penicillin once the organism has been isolated. Highdose intravenous penicillin is the drug of choice since resistance to penicillin is not an issue with GBS. Once the infection has been controlled, the parenteral regimen is replaced by an oral β-lactam agent such as penicillin or amoxicillin. Antimicrobial therapy is continued for 4–6 weeks, until all wounds are covered with split thickness skin grafts. However, in the five cases reported here there were some variations in the antimicrobial therapy administered because of the preferences of individual treating physicians. Some authors have advocated the use of clindamycin in combination with penicillin in cases of GBS necrotizing fasciitis [2, 3], and there is now growing in vitro and in vivo evidence that clindamycin may be the preferred agent for treating streptococcal necrotizing fasciitis. While not used to treat our patients, the combination of clindamycin and penicillin may be superior to penicillin alone and should be considered in the treatment of future cases of invasive GBS infections [2, 3]. Skin and soft tissue infections are the most common manifestations of invasive GBS infection [4, 5]. However, monomicrobial necrotizing fasciitis caused by GBS in non-pregnant adults is extremely rare, with just over ten cases being reported in the English-language medical literature to date [2, 3, 6–9]. The addition of the five cases we observed make clear that GBS is capable of causing necrotizing fasciitis. While the virulence factors that enable GBS to cause necrotizing fasciitis have not yet been established, this emerging clinical entity has been reported increasingly in recent years [2, 3, 6–9]. All five of our cases occurred during a relatively short period of time, between 2000 and 2002. Horizontal transfer of DNA encoding virulence factors (such as M1 or M3 surface proteins) among different strains of GAS have been demonstrated previously [10, 11]. Gardam et al. [2] postulated that a similar process may have occurred between group A and B streptococci, conferring the mutant strain of GBS with increased ability to spread through tissue planes, resulting in rapid tissue necrosis. This theory is supported by a report of the isolation of a 12,000-kD pyrogenic toxin similar to that found in GAS from a GBS strain in a case of toxic shock syndrome caused by this organism [12]. This sharing of C.-H. Wong (*) . K.-C. Tan Department of Plastic Surgery, Singapore General Hospital, Outram Road, Singapore, Singapore, 169608 e-mail: wchinho@hotmail.com Tel.: +65-63214686 Fax: +65-62209340

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