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.
A one-year-old boy presented to the emergency department with a sudden onset of fulminant edema of the right eyelid, making it impossible to open his right eye (Figure 1 ). The ophthalmologic examination showed painful eyelid edema with conjunctival chemosis. Due to the extensive eyelid swelling, it wasn’t possible to examine pupillary light reflexes or ocular motility nor to perform a fundus examination. The boy had a temperature up to 39.1°C. Physical examination showed an alert patient, without neurological or meningeal signs, but with cutaneous varicella lesions spread over his entire body.\nLaboratory work up showed normal leukocytes (9.23 x 103/µl), thrombocytopenia (platelets 67 x 103/µl) and elevated CRP (52 mg/l). The boy hadn’t received his vaccination for varicella yet, which usually takes place between the age of 12 to 15 months. Clinical examination couldn’t exclude orbital cellulitis and revealed multiple enlarged lymph nodes in the neck region. There was a clinical suspicion of a secondary bacterial infection of the cutaneous varicella lesions around the eyelid. CT of the orbit revealed pronounced superficial soft tissue inflammation of the right periorbit without evidence of an intraorbital inflammation or abscess formation, cavernous sinus thrombosis or intracranial extension of the inflammation (Figure 2 ).\nThe boy was hospitalized for a trial of intravenously antiviral (acyclovir) and antibiotic therapy (amikacin, flucloxacillin, and ceftriaxone). The antibiotic therapy was changed to clindamycin after 2 days due to poor clinical response with also increasing swelling of his left eyelid (Figure 1 ). In immunocompetent children, VZV usually causes a benign infection without the need for systemic antiviral treatment, in this case the pediatrician decided to treat the varicella infection with intravenously acyclovir for 5 days (30 mg/kg/day in 3 divided doses). The laboratory markers of inflammation raised with a maximal leucocytosis of 23.8 x 103/µl and a CRP level of 190 mg/l. There weren’t any clinical signs of sepsis. The peripheral blood count and culture of vesicular fluid obtained at the emergency department were negative. On the second day of admission, the right upper eyelid ruptured spontaneously (Figure 1 ). We removed the overlying crusts and debris and took a swab of the underlying ulcer. Culture grew the anaerobic organism Veillonella parvula, without identifying any other bacterial or fungal organisms. Clindamycin was continued to cover anaerobe bacteria. The antibiogram showed resistance to penicillin, amoxicillin clavulanic acid and even metronidazole, but sensitivity to clindamycin and meropenem. The source of infection was most likely a superinfection of the varicella skin lesion. Clindamycin was given intravenously for 3 weeks with a good clinical response showing a slow but progressive decline of the eyelid edema. When the boy was discharged from the hospital, clindamycin was continued orally for another 4 weeks, resulting in a total antibiotic treatment duration of 7 weeks. The eyelid swelling with a hardened eyelid persisted for 4 months. Because of this, the boy was unable to fully open his eye in the first 4 months, obscuring the child’s visual axis and putting him at great risk for developing occlusion amblyopia (Figure 3 ). The patient gained a full recovery with a complete resolution of the eyelid edema and a clear visual axis without need for surgical intervention. He is still in follow-up with a pediatric ophthalmologist for regular amblyopia screening and early treatment if necessary.