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Fifty pediatric cases of acute Staphylococcus aureus osteomyelitis were randomized to receive 150 mg/kg/day of cephradine divided in four doses, or 40 mg/kg/day in four doses of clindamycin. The treatment was initiated intravenously, but switched to oral administration mostly within 4 days, using the same doses. The peak antimicrobial serum inhibitory titer or bactericidal titer was not measured. The course of illness was monitored by blood leukocytes, erythrocyte sedimentation rate, and serum C-reactive protein. The follow-up was extended to 1 year posthospitalization.
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Successful management of anaerobic infection first requires an accurate diagnosis. Cytologic examination of wound exudates and inspection for characteristic clinical clues greatly facilitates an accurate initial diagnosis of anaerobic infection. Knowledge of antimicrobial activity against specific anaerobic pathogens is essential, since antibiotic susceptibility information is not routinely available. Whenever possible, antimicrobial and surgical therapy should be combined in managing anaerobic infections. Chloramphenicol, clindamycin, and metronidazole provide the most consistently reliable activity against pathogenic anaerobes, including Bacteroides. Penicillins are also generally effective, except for treatment of infections caused by penicillinase-producing strains of Bacteroides. Cephalosporins are not considered drugs of choice for anaerobic infections, although cefoxitin may in some instances be useful as monotherapy of mixed infections containing obligate anaerobes and coliform bacteria. Aminoglycosides and sulfonamides are ineffective and should be avoided for treatment of anaerobic infection.
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A 21-year-old man suffered from cough, dyspnoea and hemoptysis following accidental aspiration of petroleum. Chest x-ray and computerized tomography one day after the aspiration showed infiltrates in the lower fields. Fiberbronchoscopy revealed severe bronchitis without any signs of necrosis. Flunisolide inhalation (200 micrograms/d) and intravenous application of prednisolone (50 mg/d) and clindamycine (600 mg/d) improved pulmonary function within a few days. The infiltrates resolved over the following two weeks. This favourable result clearly shows that conservative treatment has a role in petroleum aspiration.
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The ability of strains of Bacteroides fragilis resistant to clindamycin and/or tetracycline to transfer resistance to a susceptible recipient strain in experimental subcutaneous abscesses in mice was investigated. The results indicated that such transfer took place at a frequency similar to that observed in vitro. Transfer of resistance determinants at infected sites may play a role in the epidemiology of disseminated resistance to antimicrobial agents.
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Since antimicrobial resistance in Streptococcus pneumoniae become serious problem, we have conducted the epidemiological analysis of Streptococcus pneumoniae in Gifu prefecture. We have investigated the mutations of penicillin-binding protein (PBP) cording genes, the mutations of macrolide-resistant cording genes, and antimicrobial susceptibility using broth microdilution method, for 345 strains isolated from clinical specimens between May 2006 and July 2006 at 12 clinical facilities of 5 medical area. The ratio of penicillin-susceptible S. pneumoniae (gPSSP), penicillin-intermediate S. pneumoniae (gPISP), and penicillin-resistant S. pneumoniae (gPRSP), which were judged by molecular techniques, were 7.2%, 53.5%, and 39.4%, respectively. Only 1 gPSSP strain was isolated from children under three years old. There have been regional differences of the isolation rate of gPRSP between Gifu/Chuno area (55-60%) and Tono/Hida area (23-32%) in second- or third-medical facilities. The isolation rate of PBP mutation genes, pbp2x, pbp1a and pbp2b, were 92.8%, 52.5% and 53.3%, respectively. The isolation rate of macrolide-resistant cording genes, mefA only, ermB only, and both mefA and ermB, were 30%, 50% and 8%, respectively. The strains of S. pneumoniae with both mefA and ermB mutations, increased from 4% in 2002 to 8% in 2006. The antimicrobial susceptibility of S. pneumoniae to penicillin G (PCG) showed two peaks around 0.03 and 1 microg/mL, and 89% of S. pneumoniae with minimum inhibitory concentration (MIC) value 1 microg/mL was gPRSP. The MIC values of PCG against 69% strains of gPRSP distributed between 0.25 and 1 microg/mL. There have been the decreased tendency for the differences among medical facilities in penicillin resistant strains. Although cefditoren showed the most effective antimicrobial activity in oral cephems tested, there have been the strains with MIC value of over 1 microg/mL. The MIC90 of panipenem was 0.125 microg/mL, which was the best antimicrobial activity in carbapenems. The resistant rates of clarithromycin and azithromycin were 85% and 84%, respectively. The strains with the gene mutation of ermB have showed resistant to clindamycin. The MIC90 of tosufloxacin was 0.25 microg/mL, which was the best antimicrobial activity in quinolones. We have detected 4 levofloxacin highly resistant S. pneumoniae, of which MIC value was over 32 microg/mL. Also, we have encountered the episode of the spread of S. pneumoniae in one family, which was clarified by scientific approach.
Time-kill studies examined the activities of telithromycin (HMR 3647), erythromycin A, azithromycin, clarithromycin, roxithromycin, clindamycin, pristinamycin, amoxicillin-clavulanate, and metronidazole against 11 gram-positive and gram-negative anaerobic bacteria. Time-kill studies were carried out with the addition of Oxyrase in order to prevent the introduction of CO(2). Macrolide-azalide-ketolide MICs were 0.004 to 32.0 microg/ml. Of the latter group, telithromycin had the lowest MICs, especially against non-Bacteroides fragilis group strains, followed by azithromycin, clarithromycin, erythromycin A, and roxithromycin. Clindamycin was active (MIC = 2.0 microg/ml) against all anaerobes except Peptostreptococcus magnus and Bacteroides thetaiotaomicron, while pristinamycin MICs were 0.06 to 4.0 microg/ml. Amoxicillin-clavulanate had MICs of =1.0 microg/ml, while metronidazole was active (MICs, 0.03 to 2.0 microg/ml) against all except Propionibacterium acnes. After 48 h at twice the MIC, telithromycin was bactericidal (>/=99.9% killing) against 6 strains, with 99% killing of 9 strains and 90% killing of 10 strains. After 24 h at twice the MIC, 90, 99, and 99.9% killing of nine, six, and three strains, respectively, occurred. Lower rates of killing were seen at earlier times. Similar kill kinetics relative to the MIC were seen with other macrolides. After 48 h at the MIC, clindamycin was bactericidal against 8 strains, with 99 and 90% killing of 9 and 10 strains, respectively. After 24 h, 90% killing of 10 strains occurred at the MIC. The kinetics of clindamycin were similar to those of pristinamycin. After 48 h at the MIC, amoxicillin-clavulanate showed 99.9% killing of seven strains, with 99% killing of eight strains and 90% killing of nine strains. At four times the MIC, metronidazole was bactericidal against 8 of 10 strains tested after 48 h and against all 10 strains after 24 h; after 12 h, 99% killing of all 10 strains occurred.
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Multiple large flap lacerations (2 x 3 to 60 x 60 cm) at various body sites were characteristic. Lower extremities were mostly affected (88%), followed by upper extremities (29%), and head (18%). Two-thirds of patients presented with combined injuries to the thorax or fractures. Near-drowning involved the aspiration of immersion fluids, marine and soil debris into the respiratory tract and all patients displayed signs of pneumonitis and pneumonia upon arrival. Three patients presented with severe sinusitis. Microbiology identified a variety of common but also uncommon isolates that were often multi-resistant. Wound management included aggressive debridement together with vacuum-assisted closure in the interim between initial wound surgery and secondary closure. All patients received empiric anti-infective therapy using quinolones and clindamycin, later adapted to incoming results from microbiology and resistance patterns. This approach was effective in all but one patient who died due to severe fungal sepsis. All patients displayed severe signs of post-traumatic stress response.
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A susceptibility survey of 537 strains of the Bacteroides fragilis group from eight centers in the United States was continued at the Tufts New England Medical Center in 1982. The results were compared with those of 755 organisms analyzed in 1981. Nine antimicrobial agents were tested by an agar dilution method. The respective percentages of resistance for 1981 and 1982 were as follows (%): cefoxitin, 8 and 10; moxalactam, 22 and 12; cefotaxime, 54 and 48; cefoperazone, 57 and 54; piperacillin, 12 and 7; clindamycin, 6 and 3; metronidazole, 0 and 0; chloramphenicol, 0 and 0; and tetracycline, 63 and 59. Regional differences in resistance rates were found. Declines in resistance to moxalactam, piperacillin, and clindamycin were noted at the participating hospitals. An outbreak of cefoxitin resistance was noted at the Tufts New England Medical Center, where the rate increased from 14 to 30%. The various species of the B. fragilis group had differing patterns of resistance; B. fragilis was the most susceptible species. Significant cross resistance among the beta-lactam agents was found. These data indicate the need to determine the susceptibility patterns of the B. fragilis group organisms within each hospital.
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The in-vitro activities of 20 antibiotics against 227 consecutive non-duplicate S. aureus isolates from clinical samples in KZN province, South Africa were determined by the disk-diffusion technique. Isolates resistant to oxacillin and mupirocin were confirmed by PCR detection of the mecA and mup genes respectively. PCR-RFLP of the coagulase gene was employed in the characterization of MSSA and MRSA.
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The anti-Pneumocystis carinii drug effects on mitogen-, antigen-, and interleukin-2-induced proliferative responses and on natural killer (NK) cell-mediated activity were analyzed in vivo (rats) and in vitro (normal human peripheral blood mononuclear cells). Splenocytes derived from in vivo piritrexim- and clindamycin-treated rats showed a significant inhibition of mitogen-induced proliferative responses. In vitro exposure to clindamycin, piritrexim, and pyrimethamine caused an inhibition of human T lymphocyte proliferation in response to mitogen, antigen, and interleukin-2 stimulation. Rat NK cell-mediated cytotoxic activity was not affected by the drugs, and human NK cell activity was reduced only at the highest concentration (10 micrograms/ml) of the drugs. The potential immunotoxicity of the long-term administration of these agents in humans needs further investigation.
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S. aureus two hours survival rates in polymorphonuclear leukocytes were 13.5 +/- 4.4 x 10(6), 10.5 +/- 4.0 x 10(6), 11.0 +/- 4.0 x 10(6), using polymorphonuclear leukocytes from controls and patients, with control and autologous sera respectively (p greater than 0.05). We have observed a bactericidal activity defect in polymorphonuclear leukocytes from one patient and in the sera of 7 other patients. The incubation with clindamycin (10 MIC) reduces the number of cfu/ml to 2.1 +/- 0.9 x 10(6), 1.1 +/- 0.7 x 10(6) y 1.9 +/- 1.1 x 10(6), and we also detected and additional inhibition of 81.7 +/- 7%, 70.7 +/- 17% and 79.0 +/- 4% respectively.
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The frequency of antibiotic-associated diarrhoea (AAD) and Clostridium difficile-associated diarrhoea (CdAD) was prospectively determined in a population of 2462 patients recruited from five Swedish hospitals, including divisions for infectious diseases, orthopaedics, surgery, geriatrics, nephrology and internal medicine. AAD developed in 4.9% of the treated patients. Faecal samples were obtained from 69% of patients with AAD and 55.4% were positive for C. difficile cytotoxin B. The frequency of AAD varied from 1.8 to 6.9% at the participating centres (P < 0.001). The frequency of AAD also varied considerably between medical disciplines and wards within different hospitals and was highest in the nephrology and geriatric units (6.7 and 7.1%, respectively). There was no difference in frequency of AAD when analysed with respect to gender or age. Medical interventions (laxative treatment, endoscopy and abdominal surgery) or presence of one concomitant disease (diabetes, malignancy, chronic renal disease and inflammatory bowel disease) did not significantly affect the frequency of AAD, whereas patients suffering from two or more of these illnesses had significantly (P = 0.001) higher frequencies of AAD. Patients treated with antibiotics for 3 days had a significantly (P = 0.009) lower frequency of AAD than those treated for longer periods. Treatment with cephalosporins, clindamycin or broad-spectrum penicillins was associated with an increased risk of AAD. With specimens from one centre, 62.5% of tested patients with AAD and 33.8% of asymptomatic patients were positive for cytotoxin B. Although C. difficile cytotoxin B in stool samples was significantly associated with AAD (P = 0.003), the causal relationship with diarrhoea is not always evident.