A slow outward current and a hypoosmolality induced anion conductance in embryonic chicken osteoclasts.
A prospective study was performed on all patients with an infection limited to the parapharyngeal space.
A review on the etiological profile of urinary tract infections in childhood and the sensitivity pattern of urinary pathogens in Spain is presented. Escherichia coli continues to be the main etiological agent of urinary tract infection in childhood. Consequently, its sensitivity pattern will usually determine the choice of empirical therapy. The predominance of E. coli is reduced in certain circumstances, in which the presence of other microorganisms is increased. However, the clinical information available at diagnosis does not allow accurate identification of the etiology; only staining and microscopic urine examination can help in treatment selection. In Spain, E. coli presents a high percentage of resistance to ampicillin and cotrimoxazole, whereas second- and third-generation cephalosporins, fosfomycin, aminoglycosides and amoxicillin-clavulanate maintain high sensitivity. In some areas, amoxicillin-clavulanate and first-generation cephalosporins show high levels of resistance, which can limit their empirical use.
The objective of the study was to define whether individual exposure to co-amoxiclav is a risk factor for selecting co-amoxiclav-resistant Escherichia coli in vivo. One hundred and eight patients were included in our study as soon as they were found to have a urinary tract infection (UTI) due to E. coli. Stool probes were also undertaken for some of these patients. Co-amoxiclav administration in the month before diagnosing the UTI, and any treatment to cure the current UTI were recorded for all patients. When co-amoxiclav-resistant E. coli was detected in the stools after diagnosis of E. coli UTI, isolates were compared with urinary E. coli isolates in terms of clonal relatedness, beta-lactam susceptibility and mechanisms of beta-lactam resistance. The patients who had taken co-amoxiclav in the month before the reported E. coli UTI had a significantly higher risk of being infected with co-amoxiclav-resistant E. coli. Those patients treated with amoxicillin for a current infection were at greater risk of intestinal carriage of co-amoxiclav-resistant E. coli; those treated with co-amoxiclav had a greater risk of intestinal carriage of co-amoxiclav-resistant Gram-negative bacilli than patients treated with third-generation cephalosporins or fluoroquinolones. Hence, individual exposure to co-amoxiclav is a risk factor for UTIs caused by co-amoxiclav-resistant E. coli or for carrying co-amoxiclav-resistant Gram-negative bacilli in the digestive tract.
In vitro response of 469 clinical isolates of gram-positive cocci was tested against MDL 62873 by the agar dilution method. The bacteria consisted of 407 isolates of staphylococci and 62 strains of enterococci. In vitro activity of MDL 62873 was compared with that of ampicillin, augmentin, erythromycin and vancomycin. All the isolates were completely inhibited by MDL 62873 at an MIC ranging between 0.25 and 8.0 micrograms/ml. In vitro activity of this new amide derivative of teicoplanin was far superior to that of ampicillin, augmentin and erythromycin and equal to or slightly better than that of vancomycin.
The incidence of drug-induced jaundice was 1.27 (confidence limits 0.85-1.8) per 100 000 per annum in a total of 28 patients (17 men, mean age 69 years). Antibiotics were the commonest cause of jaundice (n=21). Of these, co-amoxiclav (n=9) and flucloxacillin (n=7) caused the majority with an incidence rate per 100 000 prescriptions of 9.91 (4.6-18.0) and 3.60 (1.5-7.2), respectively. Co-amoxiclav-induced jaundice was observed more commonly in elderly males (age 65 years, M : F 7 : 2). In those patients with flucloxacillin or co-amoxiclav-induced jaundice, bilirubin ranged from 54 to 599 mumol/l (267 mumol/l) with a resolution of jaundice between 30 and 90 days. Counselling with regard to potential drug-induced liver injury and reporting of the adverse reaction had been performed in 1/28 patients.
Subgingival plaque samples from patients with periodontitis were collected and cultured on selective and nonselective culture media. The antimicrobial susceptibility of periodontopathogenic isolates was studied in chronic periodontitis patients in Colombia. Metronidazole, amoxicillin, amoxicillin/clavulanic acid, clindamycin and moxifloxacin were tested on all bacterial isolates and the percentage of resistant strains was calculated.
30 representative intrinsically penicillin-resistant coagulase-negative staphylococcal (CONS) isolates yielded discrepant agar disk diffusion test (Bauer-Kirby) results for augmentin. Clavulanic acid (2.5 micrograms/ml) enhanced the activity of amoxycillin from 8- to greater than or equal to 128-fold (mean = 26-fold); MICs of amoxycillin (combined with 2.5 micrograms/ml clavulanate) ranged from 1-16 (mean = 3) micrograms/ml. It is recommended that clinical microbiology laboratories withhold 'susceptible' augmentin disk tests results from their reports regarding intrinsically penicillin-resistant CONS isolates. No such discrepancies were encountered among clinical isolates of Staphylococcus aureus.