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 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.