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 67-year-old man with a history of treated prostate cancer, alcohol abuse and alcoholic cirrhosis presented to an urban, academic hospital with new low back pain. The pain had started 2 weeks prior to his presentation, had gradually worsened, and then became associated with bilateral lower extremity shooting pain and weakness. He denied bowel or bladder incontinence or saddle anaesthesia. He also denied subjective fevers or chills or any other bothersome symptoms. He was found to have normal vital signs, poor dental hygiene, tenderness over the lumbar spinous processes, and normal neurological and prostate exams. Magnetic resonance imaging (MRI) of the spine () showed mild compression fractures, with small lytic lesions throughout the thoracic and lumbar spine, and a large lytic lesion at the L5 vertebral body. The patient had a normal prostate specific antigen (PSA) level and a normal white blood cell count. C-reactive protein was mildly elevated at 30 mg l−1 (normal range 0–10 mg l−1).\nThere was concern for metastatic cancer given the patient's prior history of prostate cancer. His normal PSA level was not reassuring, because his prior prostate cancer had been diagnosed in the setting of a normal PSA level. He was started on intravenous dexamethasone 4 mg every 6 hours given the concern for metastatic spinal lesions and a neurosurgical consult was obtained. The neurosurgery team did not feel that urgent surgical intervention was needed and thus a biopsy of the lesion was obtained by the interventional radiology team for diagnostic purposes. Surprisingly, the vertebral biopsy result showed no evidence of malignancy, but did show findings consistent with osteomyelitis and was sent for culture. Dexamethasone was discontinued and blood cultures were drawn. Antibiotic therapy was withheld while culture data was pending, as the patient was clinically stable.\nThe patient was observed while the cultures were pending, and 2 days later Veillonella species started growing from the broth of the tissue biopsy and from one of two blood cultures. After a great deal of prompting for additional history, the patient reported a mechanical fall 4 weeks prior to the onset of his pain, at which time several teeth had been dislodged. A trans-thoracic echocardiogram obtained to evaluate for possible endocarditis was negative. Additionally, repeat blood cultures obtained to ensure clearance of the bacteraemia after the initiation of antibiotics were also negative. Culture sensitivity results were obtained, but were delayed as the sample had to be sent out to a reference laboratory for further testing. In the meantime, ceftriaxone 1 g intravenous daily was started and the patient was discharged to a nursing home for further rehabilitation, with close clinical follow-up scheduled. The sensitivity testing was performed by broth microdilution and showed that there was no β-lactamase inhibition. The MIC results showed sensitivity to meropenem, ampicillin/sulbactam and piperacillin/tazobactam, and borderline sensitivity to metronidazole and penicillin. The results were delivered with the caveat that there are currently no Clinical and Laboratory Standards Institute guidelines in the USA for the performance and interpretation of susceptibility testing for anaerobes other than Bacteroides fragilis. Thus, the advice of the reference laboratory was to interpret these results with caution. At his follow-up appointment, the patient appeared to be having a good clinical response to ceftriaxone. Given the lack of β-lactamase inhibition in the culture data and the fact that once daily dosing of antibiotics decreases disruption of therapies, ceftriaxone was continued. The patient completed a 6 week course of antibiotics and had complete resolution of his symptoms.