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Uncontrolled open-label study of atovaquone given through an expanded access programme; statistical analysis was performed on an intent-to-treat basis.
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During 31 months of study, 808 patients with polymicrobial surgical infection were randomized for antibiotic therapy between a third-generation cephalosporin (moxalactam disodium , cefotaxime sodium , and cefoperazone sodium ) and the combination of gentamicin sulfate plus clindamycin (393). Results based on antibiotic therapy included the following: cure in 83% given cephalosporin, 73% with antibiotic combination; control but recurrent sepsis in 7% and 15%; and failure in 4% and 8%, respectively. Such data support the tenet that third-generation cephalosporins are at least equal, if not superior, to the combination of gentamicin plus clindamycin for treatment of polymicrobial surgical sepsis.
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We conducted a 3-year retrospective cohort study of outpatients with cellulitis empirically treated at a teaching clinic of a tertiary-care medical center in Hawaii. Patients who received more than 1 oral antibiotic, were hospitalized, or had no follow-up information were excluded. Treatment success rates for empiric therapy were compared among commonly prescribed antibiotics in our clinic: cephalexin, trimethoprim-sulfamethoxazole, and clindamycin. Risk factors for treatment failure were evaluated using multivariate logistic regression analysis.
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This was a bicentre, open-label, randomised, three-arm phase 3 trial done in Lisungi health centre in DR Congo, and Kazo health centre in Uganda in 2012-14. Children aged 12-60 months with recurrent malaria infection after treatment with the first-line ACT were randomly assigned to either re-treatment with the same first-line ACT, an alternative ACT, which were given for 3 days, or quinine-clindamycin (QnC), which was given for 5-7 days, following a 2:2:1 ratio. Randomisation was done by computer-generated randomisation list in a block design by country. The three treatment groups were assumed to have equivalent efficacy above 90%. Both the research team and parents or guardians were aware of treatment allocation. The primary outcome was the proportion of patients with an adequate clinical and parasitological response (ACPR) at day 28, in the per-protocol population. This trial was registered under the numbers NCT01374581 in ClinicalTrials.gov and PACTR201203000351114 in the Pan African Clinical Trials Registry.
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Toxic shock syndrome (TSS) is an acute toxin-mediated illness caused by toxin-producing strains of Staphylococcus aureus and Streptococcus pyogenes. There is no recent data regarding incidence, management and mortality of TSS in UK children.
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The majority of patients hospitalized with community-associated S. aureus infections were due to MRSA, most of which involved an SSTI. African-American race, recent antibiotics and past homeless status predicted infection with MRSA; however, no clinical profile could reliably exclude MRSA. Clinicians should be aware of the increasing prevalence of CA-MRSA.
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The Gram-positive human pathogen Staphylococcus aureus causes a variety of human diseases such as skin infections, pneumonia, and endocarditis. The micrococcal nuclease Nuc1 is one of the major S. aureus virulence factors and allows the bacterium to avoid neutrophil extracellular trap (NET)-mediated killing. We found that addition of the protein synthesis inhibitor clindamycin to S. aureus LAC cultures decreased nuc1 transcription and subsequently blunted nuclease activity in a molecular beacon-based fluorescence assay. We also observed reduced NET degradation through Nuc1 inhibition translating into increased NET-mediated clearance. Similarly, pooled human immunoglobulin specifically inhibited nuclease activity in a concentration-dependent manner. Inhibition of nuclease activity by clindamycin and immunoglobulin enhanced S. aureus clearance and should be considered in the treatment of S. aureus infections.
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The two antibiotic regimens were equally effective for a clinical cure, bacterial eradication and incidence of adverse experiences.
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A multiplex PCR assay was used to detect the erythromycin (EM) and clindamycin (CM) antibiotic resistance genes, ermB, ermTR, and mefA/E, in Group B Streptococcal (GBS) clinical isolates and in DNA extracted from the corresponding cervicovaginal-rectal (CVR) swabs. We compared these results to the standard EM/CM double disk diffusion assay of 46 isolates. Given that these genes are present in other CVR flora and are found on mobile genetic elements, the PCR assay was unable to predict GBS resistance directly from the swabs. Therefore, PCR can only accurately detect resistance genes and predict the resistance phenotype from purified GBS isolates.
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An out-patient parenteral antibiotic therapy program provided through a medical day care unit was evaluated in a tertiary care hospital. From July 11, 1988 to December 31, 1990, 122 patients were treated either on site at the unit or at home with self-administered intravenous antibiotics. In all, 142 courses of parenteral antibiotics (mostly cephalosporins and clindamycin) were given for a total of 124 infections, mostly bone and soft tissue infections (67 of 124, 54%). The duration of out-patient therapy ranged from two to 62 days with a mean duration of 9.4 days if treated at the unit, or 13.2 days in the home care model (1476 patient-days). Vein access was peripheral and catheters remained functional for an average of 4.9 days (range 0.5 to 22 days). Only two patients experienced adverse drug reactions that necessitated modification of treatment. One other case was readmitted to the hospital for surgical debridement. The average cost per patient-day was $66 compared with $375 for in-hospital therapy. This program proved to be safe, efficient, and cost-effective.
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The results showed high incidence of C. difficile and also high antibiotic resistance of this bacterium, but frequency of strains containing virulence genes (tcdA, tcdB, cdtA and cdtB) was low.
The characteristics of an antibiotic that favor its ability to select for resistant bacteria are not completely understood. Otherwise, by the common use of broad-spectrum cephalosporins, resistant strains of several gram-negative species, especially Enterobacter cloacae, have been more frequently isolated. During our studies on beta-lactam resistance in E. cloacae, we observed that the addition of an inhibitor (clindamycin) to a potent inducer (cefoxitin) leads to an enhanced selection of resistant mutants. This could explain the emergence of beta-lactam resistant strains during antibiotic therapy.