Linezolid Therapy of Bloodborne Teicoplanin-Resistant Staphylococcus haemolyticus

Abstract

Coagulase-negative staphylococci (CNS) are human skin commensals, but are now also recognized as an important cause of foreign-device infections and nosocomial bacteremia [1, 2]. Staphylococcus epidermidis is the CNS species most frequently identified, followed by Staphylococcus haemolyticus, which accounts for about 10% of isolates [3]. Glycopeptides – vancomycin or teicoplanin (available in almost all European countries) – are the drugs of choice for these infections, as CNS isolated in hospitals are frequently resistant to methicillin. Diminished susceptibility and resistance to glycopeptides are both rare but have been reported in Staphylococcus aureus [4] and S. haemolyticus [5]. S. haemolyticus is an important nosocomial pathogen with a tendency to develop multiple antibiotic resistance. Linezolid is a new antibiotic licensed for the treatment of staphylococcal infections, but clinical experience in the therapy of CNS infections has been limited [6]. We describe a case of S. haemolyticus bacteremia in which teicoplanin resistance developed during treatment and which was successfully treated with linezolid. A 62-year-old woman with no past medical history was diagnosed with acute myeloid leukemia in June 2004. Fourteen days after starting the third course of chemotherapy she developed febrile neutropenia, for which she received intravenous empiric antibiotic therapy with piperacillintazobactam and ofloxacin. Clinical efficacy was poor, and two sets of blood cultures yielded a coagulase-negative Staphylococcus isolate that was identified as S. haemolyticus by using the API test system (bioMerieux, Marcy l’Etoile, France). Initial antimicrobial sensitivity testing with the API system showed that the isolates were resistant to oxacillin but susceptible to vancomycin and teicoplanin. Intravenous teicoplanin therapy was started (400 mg/daily, after a loading dose of 400 mg bid for 2 days), as a lifethreatening allergic reaction to vancomycin had occurred during the first course of chemotherapy. Her condition continued to deteriorate despite this treatment: in particular, she remained febrile and her respiratory function deteriorated. The respiratory rate was 30 breaths/min and the oxygen saturation 91% on 10 l/min oxygen. Chest radiography showed a diffuse and worsening alveolar syndrome. After 2 days of antibiotic treatment she was transferred to the medical ICU. On admission her blood pressure was 110/60 mmHg, her heart rate 100 beats/min, and her respiratory rate 32 breaths/min. Her oxygen saturation was 95% on