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• W1990370832 abstract "After pneumonia osteomyelitis is the most common systemic bacterial infection with a known focus in children with sickle cell disease (SCD).1Salmonella spp., Staphylococcus aureus and Gram-negative enteric bacilli are the usual agents causing osteomyelitis in patients with SCD.1-3 Anaerobes are an unusual cause of osteomyelitis in these or other hosts. Clostridium difficile, a Gram-positive, spore-forming obligate anaerobe, typically causes antibiotic-associated diarrhea and pseudomembranous colitis. However, it rarely is involved in extraintestinal infections, including osteomyelitis.4-8 We describe what we believe is the first case report in the English language literature of an association of SCD and C. difficile osteomyelitis of a long bone. Case report. A 15-year-old black female with SCD and frequent episodes of vasoocclusive crises was admitted to Texas Children's Hospital in December, 1994, with fever to 102°F, left knee pain for 3 weeks and inability to walk for 2 days. She denied leg trauma. She had been hospitalized with radiographic findings consistent with pneumonia or acute chest syndrome 5 weeks before admission and was treated with cefuroxime intravenously for 2 weeks and clarithromycin orally for 3 weeks. During that hospitalization she had developed fever to 103.5°F, bilateral knee pain and left knee swelling. Two blood cultures were sterile and knee roentgenograms were normal. Marked clinical improvement prompting her discharge occurred after an exchange transfusion. Physical examination at the time of admission revealed an anxious adolescent, unable to bend her left knee because of pain. The temperature was 99.4°F orally. Her left leg had diffuse, warm and tender soft tissue swelling from just below the knee to the lower third of the leg. Exquisite bony tenderness was elicited on palpation of the left proximal tibia. Her abdomen was soft with mild diffuse tenderness. The hemoglobin was 9.9 g/dl, hematocrit 29.1%, white blood cell count 10 110/mm3 and platelet count 502 000/mm3. Two blood cultures were obtained. Roentgenography revealed a diffuse permeative pattern in the upper third of the left tibia and diffuse, smoothly marginated, periosteal reaction consistent with chronic osteomyelitis. A needle aspirate of blood from the left proximal tibia was sent for culture, and intravenous nafcillin and cefotaxime were initiated. The blood and bone aspirate cultures were negative. A bone scan revealed increased uptake in the cortex and periosteum of the left tibia with relative sparing of the medulla suggestive of an intramedullary abscess. Surgical irrigation and debridement were performed on the third day of hospitalization, revealing foul smelling, grossly purulent intramedullary material and necrotic bone, extending from the proximal to the distal metaphysis of the left tibia. Three cortical windows were made along the tibia anteriorly and the incisions were left open. On Postoperative Day 2 clindamycin (40 mg/kg/day) was initiated and nafcillin was discontinued. A pure growth of C. difficile was identified from 4 of 5 intraoperative cultures taken from different sites. Histopathology showed evidence of subacute and chronic osteomyelitis. On Postoperative Day 4 vancomycin (600 mg every 12 h) and metronidazole (30 mg/kg/day) were initiated intravenously and clindamycin and cefotaxime were discontinued. Susceptibility testing revealed that the isolate of C. difficile was resistant to clindamycin, cefotaxime and cefoxitin and susceptible to penicillin G, piperacillin and metronidazole. The gastroenterology evaluation, including processing of stool specimens for bacterial pathogens, ova and parasites and C. difficile toxin assay, was negative. Abdominal ultrasonography and computed tomography showed no evidence of an intraabdominal or pelvic abscess. Upper and lower gastrointestinal endoscopy revealed moderate chronic duodenitis and mild chronic inflammation of the colon. On completion of 8 weeks of intravenous vancomycin and metronidazole therapy, chronic suppressive therapy with oral metronidazole (2 g/day) was initiated. At a 1-year follow-up visit the patient could walk without difficulty and has remained free of overt disease while receiving suppressive therapy. Discussion. Templeton et al.9 have noted that there are three distinctive clinical presentations for anaerobic osteomyelitis of long bones including an acute hematogenous form in young immunocompetent patients, superinfection of a fracture upon an existing aerobic infection, and indolent infection of a surgical site with a prosthetic device in place. In these authors' study of anaerobic osteomyelitis of long bones, 4 of 18 patients had underlying homozygous SCD and 1 patient had sickle cell-hemoglobin C disease.9 In another large review of anaerobic osteomyelitis, 2 of 201 patients had underlying SCD.10 However, patients with clostridial infection alone were excluded from these studies for unspecified reasons. Among patients with anaerobic osteomyelitis, Clostridium species are infrequent. Lewis et al.11 noted 35 isolates of Clostridium spp. in a review of 260 reported cases of nonactinomycotic anaerobic bone infection. They reported 2 more patients with Clostridium spp. as a part of a polymicrobial mixed aerobic and anaerobic infection. Brook12 identified 4 of 63 anaerobes as Clostridium spp. in 26 children with anaerobic osteomyelitis. A 10-year experience of anaerobic osteomyelitis in a military hospital identified 6 of 122 anaerobes as Clostridium spp.13 However, there was no patient with underlying SCD in any of these studies and none of the isolates was further identified as C. difficile. Our patient is the fourth reported in the English literature with C. difficile osteomyelitis. The first was a 21-year-old man who fractured his femur in a motor vehicular accident and developed chronic osteomyelitis at the site of a Kirschner nail.6 There was a concern that the organism had been acquired nosocomially. The second report involved a 77-year-old hypertensive woman with hematogenous chronic vertebral osteomyelitis.7 The third was a 30-year-old woman with SCD and frontal bone osteomyelitis, suspected by the authors to have been acquired hematogenously.8 As with our patient trauma was not a factor in the latter 2 patients. These patients had no symptoms relating to the gastrointestinal tract and the second reported patient's stool guaiac examination and barium enema were normal. Our patient did have chronic abdominal pain and known inflammation of the colon. One of the mechanisms involved in the pathogenesis of hematogenous osteomyelitis in patients with SCD is thought to be thrombotic, ischemic mucosal injury and invasion by intestinal flora.1 The finding of mild colitis in our patient suggests a similar mechanism. The fact that she was recently hospitalized and treated with antibiotics would increase her risk for colonization with C. difficile.4 A stool culture for C. difficile was not performed. The C. difficile isolate from our patient was resistant to clindamycin. In a study of in vitro antimicrobial susceptibility of 84 strains of C. difficile isolated from stools of patients with antibiotic-associated diarrhea or colitis, 60% of the strains were inhibited by clindamycin at 1 μg/ml and 9% were resistant to a concentration of 128 μg/ml. More than 95% of isolates were susceptible to vancomycin, penicillin G, ampicillin and metronidazole at concentrations of ≤4 μg/ml.14 The isolate in the first patient reported with C. difficile osteomyelitis6 developed resistance to penicillin during therapy, and this patient was subsequently treated successfully with metronidazole. The second reported patient recovered after oral metronidazole therapy7 and the patient with SCD and frontal bone osteomyelitis was treated successfully with chloramphenicol.8 We chose to treat our patient with vancomycin and metronidazole and to continue suppressive therapy with metronidazole. She remains at risk for developing a chronic draining sinus or pathologic fracture at 15 months into suppressive therapy because of the extent and chronicity of the bony infection. Osteomyelitis caused by C. difficile in patients with SCD may escape recognition if species of clostridia isolated from bone are not defined. Metronidazole seems to be effective based on the limited clinical information available and is also relatively inexpensive. Bacterial resistance to antibiotics, particularly penicillin or clindamycin, may be a potential reason for failure of medical therapy. In a patient with C. difficile osteomyelitis and SCD, gastroenterology evaluation should be considered. Acknowledgment. We thank Carol J. Baker, M.D., for a helpful review of the manuscript. Manjusha J. Gaglani, M.B.B.S.; Jeffrey C. Murray, M.D.; Ammar B. Morad, M.D.; Morven S. Edwards, M.D. Sections of Infectious Diseases (MJG, MSE) and Hematology-Oncology (JCM, ABM) Department of Pediatrics; Baylor College of Medicine; Houston, TX" @default.
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• W1990370832 title "Chronic Osteomyelitis Caused by Clostridium difficile in an Adolescent with Sickle Cell Disease" @default.
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