Extract

(See the Major Article by Shelburne III et al on pages 223–30.)

In this issue of Clinical Infectious Diseases, Shelburne et al report their development and validation of a clinical prediction model for β-lactam resistance in viridans group streptococci (VGS) causing bloodstream infection (BSI) and offer guidance for the use of vancomycin (or gram-positive spectrum antibiotics) for empiric therapy of febrile neutropenia (FN) [1]. Although VGS cause a significant minority of BSIs in FN patients, they are associated with a shock syndrome (VGSS) and/or acute respiratory distress syndrome (ARDS) in 7%–39% of patients, with mortality rates ranging from 2% to 21% [2–9]. VGSS/ARDS was initially described in the 1990s and linked to the presence of profound neutropenia, oral mucositis , high-dose chemotherapy, and also to fluoroquinolone or trimethoprim-sulfamethoxazole prophylaxis and ceftazidime empiric therapy for FN [5, 6, 8, 10, 11]. Poor in vitro activity against Streptococcus mitis, the most common cause of VGSS/ARDS, is characteristic of these antibiotics. Later-generation expanded-spectrum β-lactams with more reliable activity against VGS (and other gram-positive pathogens) have largely supplanted ceftazidime for empirical antibiotic monotherapy and include cefepime, piperacillin-tazobactam, and the antipseudomonal carbapenems, imipenem and meropenem [12, 13]. Increasingly, however, VGS bearing diminished susceptibility to penicillin and to the newer β-lactams are being recognized [2, 6, 10, 11]. These β-lactam resistant isolates primarily concern Shelburne et al as potentially causing rapid and disastrous complications from VGS bacteremia in patients with FN.

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