Treatment of a recurring infection of a pacemaker-pocket caused by methicillin-resistant staphylococcus aureus with tigecycline.

摘要

Staphylococcus aureus is one of the most common causes of nosocomial infections, but also increasing in prevalence among community-acquired infections. Resistance to methicillin among staphylococcal strains represents a growing threat in the hospital setting, particularly in surgical and intensive care patients. Tigecyclin is the first glycylcycline antibiotic available for clinical use. We report about a multi-morbid patient with recurring pacemaker-pocket infection due to MRSA, which was treated with intravenous tigecycline. Introduction Staphylococcus aureus is one of the most common causes of nosocomial infections, but also increasing in prevalence among community-acquired infections [1, 2]. Resistance to methicillin among staphylococcal strains represents a growing threat in the hospital setting, particularly in surgical and intensive care patients [3, 4]. Tigecyclin is the first glycylcycline antibiotic available for clinical use. It is approved for complicated skin, skin-structure and complicated intra-abdominal infection treatment [5]. It is active against a wide range of multi-drug resistant Gram-positive and Gram-negative bacteria, including methicillin-resistant Staphylococcus aureus (MRSA). We report about a multi-morbid patient with recurring pacemaker-pocket infection due to MRSA, which was treated with intravenous tigecycline. Case report The patient was a 70 year old caucasian female with chronically hemodialysis due to terminal renal failure since 2002. Her medical history included insulin dependent diabetes mellitus, polyneuropathy and metabolic syndrome. In 2004 a pacemaker was implanted due to sinuatrial block. Furthermore she developed bradyarrhythmia absoluta in 2006. Therefore and for deep vein thrombosis of her right leg in 2006 she was orally anticoagulated. At admission in February 2008 she presented with infection of the pacemaker pocket. No fever, no leucocytosis and only a discrete elevation of C-reactive protein (CRP) were found. Sonographically no abscess but a diffusely infiltrated tissue around the pacemaker-cables was seen. Transesophageal echocardiography showed no signs of intracardiac involvement and calculated intravenous antibiotic therapy with 1g ceftriaxon daily was initiated. During treatment for 14 days restitution of the local clinical findings occurred and the CRP-level normalized. Computed tomography showed no signs of infection in the pacemaker pocket and no involvement of the intracardial pacemaker-cables. Twelve days after the treatment the local signs of infection reoccurred and sonographically an abscess impressed. The CRP-level rose again, but there was no fever, leukocytosis or elevation of procalcitonin-level. Intracardiac involvement was again echocardio?graphycally excluded. Again calculated antibiotic therapy, this time with twice a day application of 500 mg ciprofloxacin orally was initiated. After 12 days of treatment the local clinical findings still indicated infection. Also sonographically signs of infection could still be seen around the pacemaker and now also around the cables. Echo?cardiographically no involvement of the intracardial pacemaker-cables could still be seen. A puncture of the abscess was performed and the microbiological analysis showed MRSA. The organism was multi?resistant to ampicillin, oxacillin, imipenem, ciprofloxacin and moxifloxacin, as well as intermediate to tetracycline. However it was susceptible to tigecycline, which was applied intravenously for 10 days. The initial dose of 100 mg was followed by 50 mg every 12 h. At this time the CRP-level fell (Figure 1) and local clinical findings normalized. Twelve days after the treatment no infectionsigns could sonographically (Figure 1) be found and the patient was discharged.