A 72-year-old Croatian Caucasian man was admitted to our hospital with fever of up to 40°C, inflammation of the pacemaker pocket area and progressive general weakness. Five years prior to this hospital admission, our patient was diagnosed with myelodysplastic syndrome and he had an impaired fasting glucose level that was treated with diet only. The current symptoms commenced two weeks after the implantation of a permanent pacemaker. He developed low grade fever up to 37.5°C accompanied by general weakness. On the seventh day of his disease, fever with chills rose up to 40°C and he was referred to our Department of Infectious Diseases. He denied any gastrointestinal disturbances including diarrhea or abdominal pain during or before this illness. He also denied close contact with animals and eating of undercooked meat or unpasteurized milk. He received no antibiotic therapy in the outpatient setting.
On physical examination there was painful red swelling of the pacemaker area, 15cm in diameter, with dehiscence of the surgical suture and serous leakage evident on his right chest region. His heart rhythm was regular with a systolic heart murmur, but our patient was hemodynamically stable. His arterial pressure was 140/70mmHg, and heart rate 84 beats/min. Bronchial rales were heard on the right side of his chest. Hepatomegaly and splenomegaly were not registered. Laboratory tests revealed an erythrocyte sedimentation rate of 96mm/h. His leukocyte count was 17.9×109/L (86% polymorphonuclear cells), erythrocytes 2.86×1012/L, hemoglobin concentration 9.9g/dL and platelet count 242×109/L. His C-reactive protein level was 156μmol/L, and blood glucose level 9.06mmol/L. Other blood biochemical parameters (creatinine, blood urea nitrogen, total protein, albumin, globulin, immunoglobulin, amylase, serum aspartate aminotransferase, alanine aminotransferase, bilirubin, creatine phosphokinase and alkaline phosphates) were within the reference ranges. A chest X-ray showed no pulmonary infiltrations. Transthoracic, as well as transesophageal echocardiography showed no signs of endocarditis. Blood, urine and wound swabs were obtained and vancomycin plus netilmicin introduced as empiric therapy. Swab culture of the infected region and three consecutive blood cultures revealed C. fetus. Urine, stool and pacemaker lead cultures obtained later, were negative.
Cultures of swabs and blood samples, plated on charcoal-based blood-free selective medium, incubated under microaerobic (5% O2, 10% CO2 and 85% N2) conditions at 25°C and 35°C resulted in the growth of gray, flat, irregular, spreading colonies after 48 hours.
The Gram stain showed a characteristic appearance of Gram-negative, curved to S-shaped rods. The identification of the strain was performed on the basis of conventional biochemical tests. An antibiotic susceptibility test, performed by using the E-test (PDM Epsilometer; AB Biodisc, Solna, Sweden), gave these minimum inhibitory concentrations for the following antimicrobial agents: ampicillin 0.12mg/L, tetracycline 0.25mg/L, erythromycin 0.19mg/L and ciprofloxacin 0.064mg/L. Minimum inhibitory concentration breakpoints were interpreted according to the guideline established by the British Society for Antimicrobial Chemotherapy.
Our patient was transferred to our Department of Cardiology where a local surgical incision and removal of the permanent pacemaker by simple traction were performed. The pacemaker pocket was drained and the wound closed by secondary sutures. Surgical drainage was followed by an immediate drop in the fever. According to the antibiotic susceptibility of C. fetus, therapy was switched to ciprofloxacin plus netilmicin. Our patient’s condition improved quickly following the treatment. Repeated blood cultures obtained during and at the end of the second week of therapy were negative. A new pacemaker system was re-implanted 14 days after his admission to our hospital, at the contralateral side of his thorax. Three days later, our patient was discharged from hospital. One month later, the area of cellulitis had healed completely, and there were no signs of inflammation of the contralaterally implanted pacemaker.