A 50-year-old man presented to the emergency room with several months of intermittent fever and progressive lower back pain. He described a mechanical fall one week prior to this admission. He had a medical history of alcohol abuse, intravenous drug use, hepatitis C infection, and native tricuspid valve infective endocarditis secondary to methicillin-resistant Staphylococcus aureus (MRSA) five months prior to his current hospital admission. At that time, his transthoracic echocardiogram showed a tricuspid valve vegetation measuring 11 × 6 mm with severe tricuspid regurgitation. He was partially treated with intravenous vancomycin followed by daptomycin with serial negative blood cultures. Magnetic resonance imaging (MRI) of his spine at that time showed no evidence of vertebral osteomyelitis or epidural abscess.\nTwo months prior to the current hospital admission, he presented to the emergency room with back pain. At this time, his blood cultures were positive for the growth of V. dispar, which was identified by matrix-assisted laser desorption/ionization-time of flight mass spectrometry. A transthoracic echocardiogram was performed prior to him leaving the hospital against medical advice and showed that the tricuspid valve vegetation was now smaller in size, measuring 7 × 6 mm (Figure ). He received no antimicrobial treatment at this time.\nDuring his current hospital admission, he was visibly agitated on physical examination and described significant lower back pain. His initial vital signs included a temperature of 39.5 degrees Celsius, heart rate of 120 beats per minute, respiratory rate of 20 breaths per minute, oxygen saturation of 97% on ambient room air, and blood pressure of 106/68 mmHg. His neck was supple and his neurological examination demonstrated normal tone throughout his upper and lower extremities. Strength in his right lower extremity was 3/5 for ankle plantar flexion and dorsiflexion, 2/5 for knee extension and flexion, and 3/5 for hip extension and flexion. His strength was 4/5 throughout his left lower extremity. His sensation was normal apart from decreased light touch sensation to his medial right gastrocnemius region. He had spinal and paraspinal tenderness in his mid and lower back. His reflexes were 2+ in his knees and plantars were down-going bilaterally. He had a grade III/VI systolic murmur best heard at the left lower sternal border. Air entry was equal and clear bilaterally with fine crackles to his right lower lung zone. No other peripheral stigmata of infective endocarditis were present on examination. Examination of the oral cavity showed he was missing upper teeth with overall poor dentition. Initial laboratory investigations are summarized in Table .\nHis electrocardiogram was normal. During his hospital admission, two sets of blood cultures obtained 96 hours apart were again positive for the growth of V. dispar. Given his persistent bacteremia, a transthoracic echocardiogram was performed which showed growth in the size of the vegetation previously noted on his tricuspid valve, now measuring 11 × 7 mm. There were also signs of torrential tricuspid regurgitation including a vena contracta width greater than 0.7 cm, a central jet that was filling greater than 50% of the right atrium, and a triangular-shaped continuous-wave Doppler signal which was as dense as the inflow signal along with evidence of systolic hepatic vein flow reversal (Figures , ).\nAn MRI scan of the spine showed early discitis/osteomyelitis of L3-L4 with a right paravertebral and right paracentral anterior epidural phlegmon with no abscess (Figure ). The neurosurgical team assessed the patient and recommended conservative management with ongoing antimicrobial therapy and physiotherapy, and monitoring for any worsening neurological deficits. In addition, given his poor dentition, a computed tomography (CT) scan of the brain, head, and neck was arranged, which showed no obvious evidence of an abscess collection within the neck, oropharynx, or brain. Furthermore, no septic pulmonary emboli were seen on imaging.\nSusceptibility testing was performed on his V. dispar isolate using broth microdilution and showed susceptibility to penicillin (minimum inhibitory concentration [MIC] < 0.5), amoxicillin-clavulanate (MIC < 4/2), and metronidazole (MIC < 8) compared against breakpoints according to the Clinical and Laboratory Standards Institute. He was treated with intravenous ceftriaxone for six weeks with clinical improvement noted within a few days following his admission. The patient reported near-complete resolution of his back pain and his repeat C-reactive protein level toward the end of therapy was 3.8 mg/L (normal 0.0-7.0 mg/L). Subsequently, he developed a central-line-associated bloodstream infection secondary to Candida dubliniensis with no evidence of endophthalmitis, for which he received a two-week course of intravenous caspofungin.\nA repeat MRI was arranged after his therapy which showed resolution of the anterior epidural phlegmon but interval worsening of the L3-L4 discitis/osteomyelitis with a new enhancement of the L3 and L4 facets without effusion (Figure ). A subsequent CT-guided lumbar spine biopsy of the L3/L4 region was performed, and bacterial, fungal, and mycobacterial cultures were negative. A repeat transthoracic echocardiogram was planned to establish a new baseline for his valvular anatomy given his risk of recurrent endocarditis; however, the patient left against medical advice.
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.