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Cytokine production by PBMC was determined after treatment with heat-killed P. acnes in the presence or absence of antimicrobials using a real-time PCR and ELISA. Cultured human epidermal keratinocytes were stimulated by IFN-gamma plus IL-1beta and the effects of antimicrobials were examined by using ELISA.
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We performed a retrospective cohort study of all patients seen in the Infectious Diseases clinic at a tertiary referral children's hospital from August 1, 2009 to August 1, 2011. We included patients who received ≥14 days of oral or intravenous antibiotic, antiviral, or antifungal medications. Patients receiving only prophylactic medications or human immunodeficiency virus treatment were excluded.
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The occurrence of macrolides and clindamycin resistance was 16.5% in 2005 increasing up to 69.9% in 2008. A high percentage of isolates was resistant to tetracycline through all the study period with no statistically significant annual.
Fourteen Corynebacterium coyleae isolates were recovered from 12 in-patients during a 5-years period. In six patients, the isolates were considered as clinically significant, three definite (sepsis), two probable (sepsis and soft tissue infection), and one possible (post-transfusional bacteremia). In the remaining 6 patients (all neonatal bacteremias), there was not enough data for considering the isolates as clinical significant. API Coryne identified all isolates as C. jeikeium, while Biolog GP2 correctly identified 7 out of the 14 isolates. Definitive identification was achieved in all isolates by the sequencing of a fragment of 724 to 1423 pb of 16S rDNA. Successive isolations from two patients presented identical random amplified polymorphic DNA (RAPD) profiles. All of the isolates were in-vitro-sensitive to beta-lactams, gentamicin, rifampin, tetracycline, vancomycin, linezolid, and resistant to clindamycin. Resistance to erythromycin occurred in 83.3% of isolates, all of them presenting phenotype cMLS and harboring the gene ermX.
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Trial quality assessments and data extraction were done independently by two reviewers. Study authors were contacted for additional information.
There was a great degree of polymorphism among the studied strains. The ample presence of hylB gene and the absence of the insertion element IS1548 in the hylB gene in invasive and colonizing strains, indicates that both groups of strains are potentially pathogenic.
An HIV-infected man became increasingly breathless and cyanosed while receiving clindamycin and primaquine treatment for Pneumocystis jirovecii pneumonia. He was found to have 11.4% methaemoglobinaemia and recovered with conservative management.
The impact of a subinhibitory dose of clindamycin combined with stimulation of host defences by muramyl dipeptide (MDP) in an animal model of surgical infection with Escherichia coli was studied. Both the percentage of bacteria recovered from the implantation site and the degree of bacteraemia were quantitated at timed intervals following the bacterial challenge. Neither of these parameters was significantly different in animals treated with clindamycin alone compared to placebo animals. A significant reduction in bacteraemia was observed in animals treated with a combination of MDP and clindamycin when compared to animals receiving either agent alone. Local bacterial recovery was paradoxically greater in this combined treatment group. The presence of subinhibitory concentrations of clindamycin in vivo appears to render E. coli more susceptible to the systemic effects of host defence stimulation by MDP.
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12B75, 274150; Abacavir sulfate/lamivudine, Abatacept, Ad2/HIF-1alpha, Adalimumab, Adefovir, Adefovir dipivoxil, AGN-201904-Z, AIDSVAX, Albinterferon alfa-2b, Alemtuzumab, Aliskiren fumarate, Alvimopan hydrate, Amlodipine besylate/atorvastatin calcium, Amlodipine besylate/Olmesartan medoxomil, Ammonium tetrathiomolybdate, Amodiaquine, Apaziquone, Aprepitant, Arsenic trioxide, Artesunate/Amodiaquine, Ascorbic acid, Atazanavir sulfate, Atazanavir/ritonavir, Atomoxetine hydrochloride, Atrigel-Leuprolide, Axitinib; Bevacizumab, Binodenoson, Bortezomib, Bovine lactoferrin; Calcipotriol/betamethasone dipropionate, Carisbamate, Certolizumab pegol, Ciclesonide, Conivaptan hydrochloride, CP-690550, CP-751871, Cypher; Dapivirine, Darbepoetin alfa, Darunavir, Dasatinib, del-1 Genemedicine, Denosumab, Desloratadine, Dexlansoprazole, DiabeCell, Drospirenone/ethinylestradiol, DTaP-HepB-IPV, Duloxetine hydrochloride, Dutasteride; Eculizumab, Eldecalcitol, Eletriptan, Emtricitabine, Entecavir, Eritoran tetrasodium, Ertapenem sodium, Escitalopram oxalate, Eslicarbazepine acetate, Esomeprazole magnesium, Estradiol acetate, Eszopiclone, ETEC vaccine, Etoricoxib, Exenatide, Ezetimibe; Fluticasone furoate, Fosmidomycin, Fosmidomycin/clindamycin; Glutamine; Heat Shock Protein 10, Hepatitis B hyperimmunoglobulin, HIV vaccine, Hochuekki-to, Human Albumin, Human papillomavirus vaccine; Immune globulin subcutaneous [human], IMP-321, Interferon omega, ISIS-301012, Istaroxime; Japanese encephalitis virus vaccine; Latanoprost/timolol maleate, Lenalidomide, Linaclotide acetate, Lumiracoxib, LY-517717; Malaria vaccine, MAS-063D, Meningitis B vaccine, Mepolizumab, Methylnaltrexone bromide, Micafungin sodium, MK-0822A, Morphine glucuronide, Morphine hydrochloride, Mycophenolic acid sodium salt; Natalizumab, Nesiritide, Norelgestromin/ethinyl estradiol, NT-201; Oblimersen sodium, Olmesartan medoxomil, Olmesartan medoxomil/hydrochlorothiazide, Omalizumab, Otamixaban; Paclitaxel nanoparticles, Panitumumab, Panobinostat, Parathyroid hormone (human recombinant), Parecoxib sodium, Pegfilgrastim, Peginterferon alfa-2a, Peginterferon alfa-2b, Pegvisomant, PI-88, Pimecrolimus, Pneumococcal 7-valent conjugate vaccine, Pneumococcal 9-valent conjugate vaccine, Pneumococcal conjugate vaccine, Poloxamer-188, Prasugrel, Pregabalin, Prulifloxacin; R-109339, Ramipril/amlodipine, Ranolazine, Rasburicase, rHA influenza vaccine, Ro-50-3821, Rosuvastatin calcium, Rotavirus vaccine, Rotigotine, Ruboxistaurin mesilate hydrate; Satavaptan, SC-75416, Solifenacin succinate, Sorafenib, Sugammadex sodium, Sunitinib malate, Synthetic conjugated estrogens B; Tadalafil, Talnetant, Taxus, Tegaserod maleate, Telbivudine, Temsirolimus, Tenofovir disoproxil fumarate, Tetomilast, Tiotropium bromide, Tipifarnib, Tofimilast, Tremelimumab, Trimethoprim; Udenafil, Urocortin 2; Valdecoxib, Vernakalant hydrochloride; XP-828L.
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Osteomyelitis following arthroscopic assisted anterior cruciate ligament (ACL) reconstruction has not been reported in literature. We describe an aggressive progression of septic arthritis and osteomyelitis leading to the complete destruction of the condylar region in a young non-immunosuppressed patient after reconstruction of the ACL. In addition we discuss the steps in diagnostics and our salvage procedures.
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A seven-year surveillance was done of the antibiotic susceptibility of Staphylococcus aureus isolated from patients seen in The Children's Hospital, Birmingham, Ala. There were no outbreaks of hospital-acquired staphylococcal infection during this time. Of 5,479 strains, 2,685 were from hospitalized children; 2,794 of 5,479 were from outpatients. The incidence of penicillin resistance increased from 76% to more than 85% between 1973 and 1979, with no significant difference noted between inpatient and outpatient strains. Penicillin resistance was similar, regardless of the clinical source (site of isolation) of staphylococci. Skin lesions, soft tissue, wounds, and abscess perennially accounted for the greatest proportion of isolates. Thus, skin lesions represent an important reservoir for penicillin-resistant staphylococci. Nearly all strains were susceptible to the other antibiotics tested; multiple resistance was rare. Susceptibility to clindamycin, erythromycin, cephalothin, sodium, and nafcillin sodium remained stable through the years. These agents provide effective therapeutic regimens for patients with staphylococcal infection, including those with penicillin allergy.
Our object is to determine the prevalence of group B streptococcus (GBS) carriage among pregnant women, the neonatal colonisation rate and the antimicrobial susceptibility to formulate a policy for treatment and prevention regarding perinatal GBS diseases in eastern Turkey. A total of 150 pregnant women were screened for GBS colonisation. Samples were collected from the vagina and the rectum of pregnant women, and the ear canal, throat and umbilicus of the neonates of colonised mothers. Antimicrobial susceptibility of the isolates was also investigated. GBS was isolated in at least one specimen from the 150 women in 48 cases; it was estimated that, overall, about 32% of the pregnant women and 17.3% of overall newborns were colonised with GBS. The overall rate of GBS vertical transmission was 54.2% in this study. Maternal colonisation rate was significantly higher in younger ages (p < 0.01) when maternal age of 20 years was taken as a cut-off point. All isolates were found to be sensitive to penicillin, ampicillin, cefazolin and vancomycin. Resistance to erythromycin and clindamycin were found to be 13.5 and 2.7%, respectively.
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Interethnic pharmacokinetic differences of antibacterials are likely; however, the clinical relevance of these differences is unknown and warrants further research.
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We report a case of fulminant septicemia with Bacillus cereus resistant to carbapenem. A 33-year-old man was suffering from febrile neutropenia (FN) on day 15 after the start of remission-induction therapy for biphenotypic acute leukemia under gut decontamination with polymyxin B and nystatin. Meropenem, a carbapenem, was administered according to the guideline for FN. Two days later (on day 17), he complained of severe abdominal pain, lost consciousness, went into sudden cardiopulmonary arrest, and died. Autopsy showed multiple spots of hemorrhage and necrosis caused by bacterial plaque in the brain, lungs, and liver. B. cereus was isolated from a blood sample obtained in the morning on day 17 and it was after his death that the isolated B. cereus was revealed to be resistant to carbapenem. B. cereus obtained from blood samples has been reported to be usually sensitive to carbapenem and also to vancomycin, new quinolones, and clindamycin. If B. cereus resistant to carbapem increases, our method of gut decontamination with polymyxin B and nystatin may have to be changed to one containing a new quinolone for the prevention of septicemia. Careful watching to determine whether B. cereus resistant to carbapem increases may be also important for empiric therapy, because carbapenem is often selected as the initial therapy for FN in patients with severe neutropenia.
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The effect of a kaolin--pectin antidiarrheal suspension on the bioavailability of orally administered clindamycin was evaluated by model-dependent pharmacokinetic techniques. Each subject's serum clindamycin concentration--time data in the absence of the kaolin--pectin suspension were fitted to a one-compartment open model with first-order absorption and lag time. The resulting disposition parameters were used to construct individual Wagner-Nelson absorption profiles, expressed as the cumulative relative fraction of clindamycin absorbed versus time following combined antidiarrheal--antibiotic therapy. For each subject, absorption persisted to varying degrees through 14 hr. On the average, the half-time for absorption was prolonged 20-fold (from about 16 min to more than 300 min). In contrast, extrapolation of the individual time courses of relative absorption to infinity revealed that the antidiarrheal had no effect on the extent of clindamycin absorption.
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The encapsulation of antiacne drugs in vesicular and particulate delivery systems represents an innovative alternative to minimize side effects, while preserving their efficacy. This can be obtained by the capacity of these systems to provide controlled release or to improve the drug penetration into skin or even into the pilosebaceous unit.
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Randomized clinical trial comparing 3 treatments (Trimethoprim-Sulfamethoxazole [TS], Dapsone-Trimethoprim [DT], and Clindamycin-Primaquine [CP] for Pneumocystis carinii pneumonia [PCP]).
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Obesity causes a number of changes, including an increase in volume of distribution and changes in hepatic metabolism and renal excretion. Several antibiotics have sufficient data to be able to make recommendations, whereas other antibiotics may need to make use of doses at the upper end of the recommended range, or utilize other dose modifications based on pharmacokinetic/pharmacodynamic parameters, in an attempt to reach adequate levels and achieve similar efficacy.
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During recent years the impact of different antimicrobial agents on the intestinal microflora in patients undergoing colorectal surgery has been investigated by our research group. Thus the effects on the microflora by parenteral administration of piperacillin, cefoxitin, cefbuperazone, moxalactam, aztreonam, imipenem, ampicillin + sulbactam, clindamycin, tinidazole, ciprofloxacin and ofloxacin have been studied. Pronounced changes were observed in the aerobic microflora in patients receiving ciprofloxacin and ofloxacin, in the anaerobic microflora in patients receiving clindamycin and tinidazole and in both the aerobic and anaerobic microflora in those patients receiving piperacillin, cefoxitin, cefbuperazone, moxalactam, aztreonam, imipenem and ampicillin + sulbactam. Postoperative infections were observed in patients receiving piperacillin (2), ampicillin + sulbactam (1), cefoxitin (1), aztreonam (3), tinidazole (6), clindamycin (5) and ofloxacin (5). In the patient groups receiving cefbuperazone, moxalactam, imipenem and ciprofloxacin, no postoperative infections occurred.
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Toxic shock syndrome (TSS) is a serious disorder with a worldwide prevalence of approximately 3/100,000 persons. TSS is mainly caused by Streptococcus pyogenes or Staphylococcus aureus. Thus, beta-lactam and lincosamides, such as clindamycin, are the first-line drugs. Yet, the mortality rate remains unacceptably high; highlighting the role of bacterial toxin-mediated activation of the inflammatory cascade in TSS pathogenesis. Further strategies should be targeted towards interfering with the interaction between bacterial toxins and host T cells. This paper aims to provide an overview of the epidemiology, pathomechanisms, and clinical presentation of TSS, and criteria for selecting drugs among available antibiotics.
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Bacterial vaginosis (BV) is the main cause of vaginitis. The condition is characterised by an abundant and odorous vaginal loss, but more than half the patients with demonstrable signs of BV do not report symptoms at all. Gardnerella vaginalis (Gv) is often associated with BV, but it is not the sole factor responsible, as is shown by the fact that it can be isolated in the vagina of women withBV. In 1992 and 1993, 2630 patients, 1460 of them gynaecological and 1170 obstetric, were admitted to the Obstetrics and Gynaecology Clinic of Parma University. Amsel criteria were adopted for diagnosing BV. Cases of BV were treated with 5 mg/die 2% clindamycin vaginal cream for 7 days. In the event of recurrences, 250 mg tablets of metronidazol were added: 8 tablets in 4 administrations in a single day, treatment also being extended to the partner. Patients admitted in 1993 received a protocol of hygienic and behavioural standards, stress being laid on prophylaxisa measures even after the end of therapy. BV proved to be present in 12.3% of cases, of whom only half were symptomatic. The situation was practically stationary if the 2 years are considered separately. Recurrences of symptomatic bacterial vaginosis were 15% in the absence of protocol application and 8.3% after the protocol. Recurrences were less frequent in the asymptomatic forms. Compared to the total number od cases of BV, recurrences were significantly low (12.1% p < 0.001).