A 72-year-old Greek woman with a medical history of serious allergic reaction to penicillin, chronic back pain, and hypertension well controlled on diuretic therapy, underwent a surgical operation for lumbar spinal stenosis, due to spondylolisthesis in lumbar vertebra 5 (L5), using instrumentation. She is a retired public employee and lives with her husband in a city in Northern Greece. She had not recently traveled outside Greece and she had no recent prior injuries. She did not drink alcohol, smoke tobacco, or use illicit drugs. On arrival, her arterial pressure was 135/80 mmHg and her other vital signs were normal. Her lungs were clear, and her heart sounds had a regular rhythm and were normal. Bowel sounds were present, and her abdomen was soft and tender on palpation. There was no rash or edema. Urine analysis was performed on admission and results were within the normal range. A neurological examination was performed with no abnormal findings: examination of cranial nerves; motor, sensory, reflex, and coordination assessment; examination of gait and station; and examination of mental status. During the operation, a discectomy was performed for a symptomatic disc herniation at thoracic vertebra 12–lumbar vertebra 1 (T12–L1). She did not receive prophylactic antibiotic treatment prior to surgery. Despite normal postoperative recovery, she was febrile on the second day (temperature up to 38.5 °C) with no clinical site of infection. Her white blood cells (WBC) count and C-reactive protein (CRP) were elevated: WBC count 14.61 cells/μL, CRP 10.2 mg/dL with normal reference range of 0.0 to 0.8 mg/dL. Remaining laboratory values were as follows: hemoglobin (Hb) 11.5 g/dL, platelets 165,000/mm3, blood glucose 98 mg/dL, serum sodium (Na) 142 mEq/L, serum potassium (K) 4.3 mEq/L, serum creatinine 0.9 mg/dL, total bilirubin 0.9 mg/dL, serum glutamic oxaloacetic transaminase (SGOT) 30 U/L, and serum glutamic pyruvic transaminase (SGPT) 26 U/L. Empirical therapy with levofloxacin was initiated; it was preferred due to her drug-allergy history. Blood and urine cultures were negative. A chest X-ray (CXR) was normal. She was afebrile by the fifth postoperative day and laboratory tests were normalized. She was discharged from hospital and continued levofloxacin 500 mg orally twice daily for 7 more days. She returned 30 days later with low grade fever (maximum temperature of 37.9 °C) and severe back pain that needed opiate analgesics. Her CRP was re-elevated (10.3 mg/dL). A magnetic resonance imaging (MRI) of her lumbar spine was performed that revealed facet joint surfaces of T12 and L1 vertebrae abnormalities, hypointense signal at T1-weighted images, and hyperintense signal in inversion recovery (IR) images. The T12–L1 disc showed hyperintense T2-weighted images signal. Intravenous contrast agent administration, revealed pathological signal at the facet joints and intervertebral disc characterized as inflammatory response. At the subcutaneous and soft tissue around the surgical intervention field, multicystic fluid areas could be observed. Post-intravenous paramagnetic contrast substance, ring formation around the fluid cysts and inflammatory response (signal enhancement) of the epidural soft tissue could be observed. No abnormal signal from the rest of the vertebrae was reported. A bone biopsy was performed under fluoroscopy guidance. A. baumannii was isolated from all five cultures obtained (bone and soft tissue derived). A. baumannii was susceptible merely to gentamicin with a minimum inhibitory concentration (MIC) <2, to imipenem with a MIC of 1, and colistin with a MIC <4, and resistant to all other antibiotic agents tested. Tigecycline (MIC 0.75) susceptibility was performed by Etest (AB Biodisk; Solna, Sweden); breakpoints were inferred from the available literature for Enterobacteriaceae (<2.0 is susceptible) as no current Clinical and Laboratory Standards Institute breakpoints are established. Despite our patient’s allergy history, she was originally administered imipenem intravenously, but she developed high fever, rash, and respiratory discomfort which were treated as an allergic reaction with H-1 histamine blockers and corticosteroids. Subsequently, tigecycline (50 mg twice a day, after loading dose of 100 mg) replaced imipenem and gentamicin (1 mg/kg administered intravenously three times a day) was added. Five days later, she developed severe vertigo and we decided to withdraw gentamicin. She could not walk or do any other physical activity due to severe pain, but she refused any kind of surgical intervention that was suggested to her. Because of the lack of available data on the role of tigecycline in the treatment of osteomyelitis, especially for an infection caused by A. baumannii, we decided to double the dose of tigecycline (100 mg twice daily) after notifying our patient of the potential risks of higher doses of tigecycline (increased probability of developing tigecycline’s side effects such as nausea, vomiting, diarrhea, abdominal pain, pruritus, rash, headache, hepatotoxicity). She consented prior to starting enhanced dosage of tigecycline. She had no adverse reactions and tolerated the regimen well, apart from slight nausea the first 2 days, which was managed with metoclopramide 10 mg administered intravenously. She was afebrile after 15 days and 30 days later she requested less opiate analgesics. Her CRP and erythrocyte sedimentation rate (ESR) were still elevated: CRP 5.7 mg/dL and ESR at 70 mm/hour. A new MRI, 30 days post the initiation of treatment with tigecycline revealed partial improvement in the soft tissue. She still refused any surgical intervention. She continued conservative therapy with high dosage for another 30 days, but then she developed severe hypoalbuminemia (serum albumin measuring at 1.9 g/dL while baseline serum albumin was 3.8 g/dL) and peripheral edema that resolved after reducing the dose to 50 mg twice daily. After completing 75 days of therapy, she could walk again and was free of analgesics, although her CRP and ESR were not yet normal. She was discharged from our hospital and continued tigecycline administered intravenously at home for a total 102 days. She had no infection relapse (clinical or radiographic signs) 18 months after the end of therapy and her CRP and ESR levels were finally normalized. Her remaining laboratory values were as follows: Hb 12.1 g/dL, WBC 5.4 cells/μL, platelets 283,000/mm3, blood glucose 88 mg/dL, serum Na 145 mEq/L, serum K 4.1 mEq/L, serum creatinine 0.8 mg/dL, total bilirubin 0.7 mg/dL, SGOT 35 U/L, and SGPT 29 U/L.