Metabolically deficient methicillin-resistant Staphylococcus aureus as cause of chronic post-thoracotomy sternal wound infection.

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Sternal dehiscence, deep wound infections and mediastinitis are serious complications of median sternotomies, occurring in 0.3–5% of cases [1]. Staphylococcus aureus and Staphylococcus epidermidis are the most common pathogens in this setting [2], and in one report the annual incidence of methicillin-resistant Staphylococcus aureus (MRSA) post-thoracotomy wound infection was below 1% [3]. We report here the case of a chronic postthoracotomy wound infection of more than 2 years’ duration from which a MRSA strain was isolated repeatedly. Remarkably, the strain persisted as a metabolically deficient mutant that differed from the known small colony variants (SCVs). A 75-year-old woman with coronary heart disease was admitted to our hospital for coronary bypass operation. Her medical history revealed diabetes mellitus type II, hypertension, and varicosis as preoperative risk factors for sternal wound dehiscence. After median sternotomy, three aortocoronary bypasses were constructed using parts of the radial artery and both internal thoracic arteries. Cefuroxime was given as perioperative prophylaxis. After bypass surgery, the patient developed a suprasternal wound infection. A swab taken from the wound grew MRSA (isolate 1); however, MRSA was not detected at other anatomical sites such as nares or skin. Antibiotic treatment with vancomycin, rifampin, and fosfomycin administered for over 1 month failed to eradicate the pathogen. Surgical wound debridement was performed at month 3 and month 4 post-surgery because of persisting sternal wound dehiscence. On both occasions, intraoperative swabs were obtained and subsequently grew MRSA; both strains were identical to isolate 1. The histopathologic characterization of an intraoperative sternal biopsy showed signs of acute osteomyelitis. A second course of antibiotic treatment with vancomycin, rifampin, and fosfomycin again failed to eradicate the MRSA. One year following bypass surgery a third surgical debridement was performed along with resection of a fistula, and at 2 years and 5 months post-surgery surgical debridement was performed for the fourth time. Intraoperative biopsy from the fourth surgical debridement grew an atypical staphylococcal isolate (isolate 2). Isolate 1 exhibited the typical growth behavior of S. aureus on Columbia agar. After 24 h at 37°C the isolate grew as yellow-pigmented colonies measuring 1.2– 1.8 mm in diameter with hemolysis, and a yellow halo was visible on mannitol-salt agar (Oxoid, Basingstoke, UK). The reactions for clumping factor (Slidex Staph Kit; bioMerieux, Marcy l’Etoile, France) and DNAse were positive. Biochemical testing with the ATB32 Staph kit (bioMerieux; numerical code: 16733260) and detection of the nuc gene by PCR confirmed the identification [4]. Susceptibility testing was performed according to the guidelines of the National Committee for Clinical Laboratory Standards [5], and two subtypes of the isolate were identified: subtype A was susceptible to trimethoprimsulfamethoxazole (TMP-SMX) and mupirocin, while subtype B was resistant to TMP-SMX and mupirocin (MIC>1,024 μg/ml). Minimum inhibitory concentrations were determined using the E-test (AB BIODISK, Dalvagen, Sweden). Both subtypes of the isolate were resistant to methicillin (MIC>256 μg/ml). The presence of the mecA gene in both subtypes was verified using the polymerase chain reaction as described by Unal et al. [6]. Isolate 2 showed quite a different phenotype; after 24 h at 37°C, it grew as yellow-pigmented colonies measuring 0.3–0.4 mm in diameter with minimal hemolysis. On mannitol-salt agar tiny colonies formed without a yellow halo. Tests for catalase and DNAse production were A. Roggenkamp (*) . A. Haas . W. Eder . H. Hoffmann Max von Pettenkofer Institute for Hygiene and Medical Microbiology, Ludwig Maximilian University Munich, Medical Centre Groshadern, Marchioninistrasse 15, 81377 Munich, Germany e-mail: andreas.roggenkamp@med.uni-muenchen.de Tel.: +49-89-218078202 Fax: +49-89-218078207