A 49-year-old Saudi man, a known case of insulin-dependent diabetes mellitus (IDDM), hypertension and ischemic heart disease, presented to the emergency department with a three-day history of fever, chills and ankle pain after trauma to his left foot. He reported a nonhealing ulcer on his left heel following a hot surface injury 20 days prior to his presentation. On examination, our patient looked ill and septic, with minimal ambulation. His temperature was 38.9°C and his blood pressure and pulse were 140/90mmHg and 108 beats/minutes respectively. A lower limb examination revealed bilateral decrease of sensation and a foot ulcer on his left heel. Careful examination of his left foot showed a 7×5cm deep ulcer on the lateral side that looked badly infected with change of skin color and profuse pus discharge. Our patient was seen by the orthopedic surgeon and an urgent extensive wound debridement involving the bone was undertaken. Blood, pus and bone tissue specimens were collected and sent to the microbiology laboratory for culture and sensitivity testing. A laboratory examination showed a white cell count (WBC) of 29×109g/L with 90% neutrophils, hemoglobin of 6.9g/L, and an erythrocyte sedimentation rate (ESR) of 97mm/h. His serum creatinine was 123umol/L, and urea mmol/L 8.9. His liver function test results were within normal limits except for serum alkaline phosphatase (ALP), which was raised (785IU/L). A left foot X-ray revealed soft tissue swelling, gas formation and fracture of the calcaneus bone. A left foot magnetic resonance imaging (MRI) scan revealed a calcaneus fracture with high suspicion of calcaneus anterior fragment osteomyelitis (Figure \n). An MRI scan of his right foot revealed mild neuropathic arthropathy (Charcot joint) with no evidence of osteomyelitis. Our patient was started empirically on intravenous ciprofloxacin 400mg twice daily, and intravenous clindamycin 600mg eight hourly. During the first three days after starting treatment, our patient showed no clinical improvement and he continued to run a low-grade fever. A pus culture grew Escherichia coli sensitive to ciprofloxacin, imipenem, meropenem, gentamicin and Enterococcus avium sensitive to ampicillin. A bone and tissue biopsy grew Morganella morganii sensitive to gentamicin, imipenem and resistant to ciprofloxacin, ampicillin, amoxicillin-clavulanic acid, piperacillin/tazobactam and cotrimoxazole. No growth occurred on the anaerobic plates despite prolonged incubation. Based on culture results, the initial antibiotics were suspended and our patient was started on imipenem 500mg intravenously (IV) six hourly, vancomycin 1g IV 12 hourly, and colistin 2 million units IV eight hourly. The blood culture obtained before treatment initiation, which was inoculated in an anaerobic bottle (Bactec Lytic/10, Anaerobic/F, Beckton Dickinson, Franklin Lakes, NJ, USA) and processed by an automated blood culture system (Bactec FX, Beckton Dickinson), grew very scanty Gram-negative cocci within 18 hours shown on Gram stain. The blood then was subcultured on Trypticase soy agar with sheep blood (BBL Microbiology Systems, Cockeysville, MD, USA) and incubated at 35°C in 5% CO2, in an anaerobic GasPak™ jar (BBL Microbiology Systems). After 48 hours of anaerobic incubation, the blood agar grew slow-growing tiny colonies (Figure \n) that showed Gram-negative cocci on Gram stain (Figure \n). The organism was identified by the Vitek 2 automated system (bioMérieux, Marcy-l'Étoile, France), as Veillonella species with a 99% probability rate. It was sensitive to imipenem (1.5μg/ml), clindamycin (0.047μg/ml), ceftriaxone (8μg/ml) and colistin, and resistant to penicillin (>32μg/ml), vancomycin, erythromycin and metronidazole. Further identification to species level and genotyping was unable to be performed, as the subcultured isolates failed to grow and the significant time delay before attempting to reisolate the organisms from the blood culture bottle rendered them nonviable. Over the subsequent five days, our patient’s condition worsened with a high temperature (38.9°C), rigors, a high WBC and ESR count. The wound was reevaluated by the surgical team and a decision of above-knee amputation was taken. Colistin and vancomycin were discontinued and imipenem was continued for four weeks. On follow-up, our patient showed gradual improvement of his condition and was discharged.
A 79-year-old man presented with a 1-month history of constant lower back pain (LBP) radiating to the right thigh. The pain had been increasing over time. Movements aggravated the symptoms. The patient reported 10 out of 10 points in the visual analog scale. He was afebrile but reported intermittent chills at night. There was no history of recent gastrointestinal procedures, dental diseases/procedures, oncological diseases, immunodeficiency, diabetes, or intravenous drug use.\nOn examination, the lumbar paravertebral muscles were tender, hip flexion on the right side revealed slightly paresis (M4/5), and minimal movement of the spine or the limbs was accompanied by severe pain.\nOn admission, the inflammation markers were elevated (C-reactive protein [CRP] 54,4 mg/l, white blood cells [WBC] count = 13,6 G/l, platelet count = 344 G/l). X-ray and a ct-scan of the lumbar spine revealed destruction of the intervertebral space L3/4 and the corresponding endplates. Because of the bony destruction, the L4-body presented an anterior wedging. The standing X-ray revealed a segmental kyphosis as a result of the wedge deformity of L4-body and the collapsed disc space L3/4 []. Blood cultures taken on admission were negative. During the next 12 h, the pain got worse, and the patient developed urinary retention, which required a bladder catheterization. MRI-scan of the lumbar spine 12 h after admission revealed an advanced spondylodiscitis L3/4 with a liquefied disc, blurred endplates, and a collection of two abscesses in the right psoas muscle. Furthermore, a diffuse signal enhancement in both psoas muscles and the autochthone muscles from L3 to S1 [] was shown. A ct-guided fine needle biopsy was performed, and the empiric intravenous antibiotic therapy with amoxicillin/clavulanate 2.2 g 4 times daily intravenously (iv.) was initiated. As the results of the biopsy did not show any growth of bacteria amoxicillin/clavulanate was stopped. After an antibiotic-free interval of 5 days (9 days after the CT-guided biopsy), an open transpedicular biopsy was performed. On the same day, iv. amoxicillin/clavulanate was resumed. The bacteriological examinations on aerobic/anaerobic cultures showed no results. The eubacterial PCR (16S rDNA-sequencing) revealed V. parvula as the causing pathogen. The antibiotic therapy was switched to ceftriaxone 2 g iv. and metronidazole 500 mg i.v. A CT of the abdomen was performed on day 21, which showed increasing abscess collection in the right psoas major of 4.1 × 4.6 cm [] but no signs of intraabdominal malignancy. A drain was inserted into the right psoas muscle, and the abscess formation was subsequently drained for 4 days.\nAbnormal high calcium levels revealed an incidental parathyroid adenoma, which had to be removed surgically. Because of the additional surgery, the patient was discharged on day 27. On day 39, the patient presented himself in good health and pain-free to our outpatient clinic. Inflammation markers had normalized (CRP 2 mg/l, normal WBC count). A small residual abscess collection in the right psoas muscle was discovered on CT scan. The CT-scans and the standing X-rays of the lumbar spine showed no instability of the spine without any progression of the kyphotic deformity L3/L4. The antibiotics were switched to amoxicillin/clavulanate 1 g po 3 times daily for another 2 weeks, completing 6 weeks of the antibiotic treatment altogether. The patient presented himself to the last follow-up at day 95 in perfect shape, without any symptoms, and further changes in the lumbar spine X-rays [].\nThere was no external immobilization of the spine during the whole duration of the treatment.