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Outcome data were abstracted from patients' medical records including infection at the surgical sites and distant nonsurgical sites and flap site complications including flap compromise, dehiscence, or fistula. Multivariate logistic regression was used to determine the association of risk factors with the primary outcome of any infection within 30 days of surgery.
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Nasal swabs of 100 healthy dogs were obtained in 2011 in Tunisia and tested for Staphylococcus pseudintermedius recovery. Antimicrobial resistance profile and virulence gene content were determined. Multilocus-sequence-typing (MLST) and SmaI-pulsed-field gel electrophoresis (PFGE) were investigated. S. pseudintermedius was recovered in 55 of the 100 tested samples (55 %), and one isolate per sample was further studied. All 55 S. pseudintermedius isolates were susceptible to methicillin (MSSP) but showed resistance to the following antimicrobials (% resistant isolates/resistance gene): penicillin (56.4/blaZ), tetracycline (40/tetM), trimethoprim-sulfamethoxazole (23.7), fusidic acid (9), kanamycin (3.7/aph(3´)-Ia), erythromycin-clindamycin (1.8/erm(B)), streptomycin (1.8/ant(6)-Ia), chloramphenicol (1.8) and ciprofloxacin (1.8). The following toxin genes were identified (% of isolates): lukS/F-I (98.2), expA (5.5), se-int (98.2), sec canine (1.8), siet (100), sea (5.5), seb (3.6), sec (10.9), sed (54.5), sei (5.5), sej (29.1), sek (3.6), ser (9.1), and hlg v (38.2). Ten different sequence-types were detected among 11 representative MSSP isolates: ST20, ST44, ST69, ST70, ST78, ST100, ST108, ST160, ST161, and ST162, the last three ones revealing novel alleles or allele combinations. Eleven different PFGE-patterns were identified in these isolates. The nares of healthy dogs could be a reservoir of antimicrobial resistant and virulent MSSP, highlighting the presence of the recently described exfoliating gene expA and several enterotoxin genes.
Clindamycin is commonly prescribed to treat children with skin and skin-structure infections (including those caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA)), yet little is known about its pharmacokinetics (PK) across pediatric age groups. A population PK analysis was performed in NONMEM using samples collected in an opportunistic study from children receiving i.v. clindamycin per standard of care. The final model was used to optimize pediatric dosing to match adult exposure proven effective against CA-MRSA. A total of 194 plasma PK samples collected from 125 children were included in the analysis. A one-compartment model described the data well. The final model included body weight and a sigmoidal maturation relationship between postmenstrual age (PMA) and clearance (CL): CL (l/h) = 13.7 × (weight/70)(0.75) × (PMA(3.1)/(43.6(3.1) + PMA(3.1))); V (l) = 61.8 × (weight/70). Maturation reached 50% of adult CL values at ~44 weeks PMA. Our findings support age-based dosing.
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Out of 413 samples collected, 128 (30.9%) were positive with GBS. The susceptibility testing revealed that 100% of isolates were sensitive to penicillin, ampicillin, vancomycin and high level gentamicin. Erythromycin and clindamycin resistance was 21.1 and 17.2%, respectively, in which 69% had harboured constitutive macrolide, lincosamide and streptogramin B (MLS(B)), 17.4% had inducible MLS(B). The M and L phenotypes were present in 6.8% each. The methylation of target encoded by ermB genes was the commonest mechanism of resistance observed in 55% of isolates, 38% of isolates had both ermB and linB genes and efflux pump mediated by mefA genes was also distributed among the isolates.
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189 bacterial strains were investigated for their in vitro sensitivity against ceftazidime (alone and in combination with another antibiotic). Moreover, the possibility to prevent development of secondary bacterial resistance as observed in subcultures at subinhibitory antibiotic concentrations, was studied using specific antibiotic combinations. Of 115 staphylococcal strains (91 strains of Staphylococcus aureus, 24 strains of Staphylococcus epidermidis), 2% were sensitive, 82% were moderately sensitive and 16% were resistant to ceftazidime. On combining ceftazidime with vancomycin, synergism was found in 61% of the strains, and secondary resistance to ceftazidime could be prevented with this combination. The combination of ceftazidime and clindamycin showed synergism in 26% and an additive effect in 48% of the strains. Secondary resistance to ceftazidime did not develop with this combination in subcultures at subinhibitory concentrations in which loss of activity was only minimal with clindamycin alone. Rifampicin and fusidic acid were highly active against staphylococci. In combination with ceftazidime, only weak synergism or additive effects were seen in most strains; no antagonism could be observed. In subcultures at subinhibitory concentrations, secondary resistance to rifampicin and fusidic acid developed rapidly and could be partially prevented by adding ceftazidime. Of 60 Pseudomonas aeruginosa strains, 84% were sensitive, 13% were moderately sensitive and 2% were resistant to ceftazidime. Synergism was most frequently observed when ceftazidime was combined with tobramycin. Using this combination, secondary resistance of Pseudomonas strains to ceftazidime did not develop. When ceftazidime was combined with piperacillin, synergism was observed in most strains, but the development of secondary resistance in vitro was not prevented.(ABSTRACT TRUNCATED AT 250 WORDS)
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Granulomatous inflammation is a common component of many diseases. In this study the ability of commonly used antibiotics to inhibit an in vitro model of granuloma formation were studied. The effect of protein kinase C inhibition in this system was also investigated.
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The comparative in-vitro activity of A-56268 (TE-031), a new semisynthetic macrolide antibiotic, was assessed against approximately 400 bacterial isolates. The new drug demonstrated excellent activity against penicillin-susceptible streptococci (MIC90s less than or equal to 0.06 mg/l) and methicillin-susceptible staphylococci (MIC90 = 0.25 mg/l). Among other Gram-positive organisms tested, a significant number were resistant to A-56268 as well as to erythromycin and clindamycin. A-56268 was at least as active as erythromycin against Pasteurella multocida and Campylobacter jejuni, but was more active than erythromycin against Legionella spp. (MIC90 less than or equal to 0.06 mg/l), Bacteroides fragilis (MIC90 = 4 mg/l) and Bact. melaninogenicus (MIC90 less than or equal to 0.125 mg/l). Activity of A-56268 was pH dependent (more active at pH 7 than at pH 6) and was moderately affected by inoculum size. The drug was bactericidal against two strains of Streptococcus pyogenes tested, but exerted a bacteriostatic effect against Staphylococcus aureus and Str. faecalis.
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In the aftermath of a methicillin-resistant Staphylococcus aureus (MRSA) ST22 hospital outbreak, we investigated the prevalence of long-term carriage, the efficacy of MRSA decolonization treatment (DT) and the spread of MRSA to households of patients and healthcare workers (HCWs). Furthermore, we evaluated the efficacy of repeated DT in long-term MRSA carriers. Of 250 index persons (58 HCWs and 192 patients), 102 persons (19 HCWs and 83 patients) and 67 household members agreed to participate. Samples from all 169 persons were taken from the nose, throat, wounds and devices/catheters, and urine samples were additionally taken from index persons. Samples from companion animals (n = 35) were taken from the nostrils and anus. Environmental sites (n = 490) screened were telephone, television remote control, toilet flush handle, favourite chair and skirting board beside the bed. Sixteen (19%) patients and two household members, but no HCWs, were ST22-positive. The throat was the most frequent site of colonization. In a multivariate analysis, chronic disease (p <0.001) and pharyngeal carriage (p <0.001) were associated with long-term MRSA carriage. MRSA was found in the environments of four long-term carriers. All animals tested were negative. MRSA-positive households were decolonized using nasal mupirocin TID and daily chlorhexidine body and hair wash for 5 days. Pharyngeal MRSA carriers also received fucidic acid (500 mg TID) combined with rifampicin (600 mg BID) or clindamycin (600 mg BID) for 7 days. The home environment was cleaned on days 2 and 5. At the end of follow-up, ten of 16 long-term carriers and the two household contacts were MRSA-negative. In conclusion, decolonization of MRSA carriers is possible, but should include treatment of household members and the environment.
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Staphylococcus species are the most common organisms responsible for infection following implantable cerebrospinal fluid (CSF) diversionary procedures. The role of an antibiotic-impregnated shunt (AIS) system in the prevention of shunt infection has remained unclear because no human clinical trial has been reported on thus far. In this study, the authors assess an AIS system with respect to its prevention of shunt infection.
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Clindamycin phosphate in dosage of 15 mg/kg was administered intravenously to dogs. Serum and pancreatic juice clindamycin concentrations were assayed. Pancreatic juice clindamycin concentrations varied between 1.32--5.5 micrograms/ml. Clindamycin was still detectable in the pancreatic juice 4 1/2 h after its administration. Clindamycin, in combination with other antimicrobials, may be potentially effective in the prophylaxis and therapy of some of the infectious complications associated with pancreatitis.
Prior colonisation of clindamycin-treated hamsters with non-toxigenic strains of C. difficile protected them from subsequent colonisation with a toxigenic pathogenic strain. In total, 13 of 18 'protected' hamsters survived for up to 27 days whereas all 27 animals challenged with the toxigenic strain alone died within 48 h. Protection was not evident if a heat-killed suspension was used or if the colonising non-toxigenic strain was first removed with vancomycin. No antitoxic activity could be detected in the faeces of animals colonised with the non-toxigenic strains. Other species of clostridia did not protect against the lethal effects of subsequent exposure to the toxigenic strain. Conversely, non-toxigenic strains would not protect the animals from the lethal effects of a different clostridial pathogen, C. spiroforme. In most cases, even in the protected animals, the toxigenic strain eventually became dominant and caused disease, with translocation across the gut wall occurring early in the disease process. It was also shown that a non-toxigenic strain of C. difficile can adhere to gut mucosa. It is proposed that the protection afforded by the non-toxigenic strains may be due to competition for ecological niches.