Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q29983 (MIC)
 21,138 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infections with enterococci that are resistant to multiple antibiotics are an emerging clinical problem. We evaluated the antibiotic treatment of experimental enterococcal endocarditis caused by two strains with different mechanisms of penicillin resistance. Enterococcus faecalis HH-22 is resistant to aminoglycosides and penicillin on the basis of plasmid-mediated modifying enzymes; Enterococcus raffinosus SF-195 is susceptible to aminoglycosides but is resistant to penicillin on the basis of low-affinity penicillin-binding proteins. Animals infected with strain HH-22 received 5 days of treatment with the following: no treatment; daptomycin (20 mg/kg of body weight twice daily [b.i.d.], intramuscularly [i.m.]), vancomycin (20 mg/kg b.i.d., intravenously), or ampicillin (100 mg/kg three times daily, i.m.) plus gentamicin (2.5 mg/kg b.i.d. i.m.). Although vancomycin was superior to ampicillin-gentamicin (P less than 0.01), daptomycin was significantly better than all other treatment regimens (P less than 0.01) in reducing intravegetation enterococcal densities, although no vegetations were rendered culture negative by this agent. Animals infected with strain SF-195 received 5 days of no therapy, ampicillin, ampicillin-gentamicin, vancomycin, or daptomycin (all at the dosage regimens described above). Daptomycin, vancomycin, and ampicillin-gentamicin each lowered intravegetation enterococcal densities significantly better than did ampicillin monotherapy or no treatment (P less than 0.01); moreover, these three treatment regimens rendered significantly more vegetations culture negative than did ampicillin monotherapy or no treatment (P less than 0.05). Serum daptomycin levels remained above the MICs and MBCs for both enterococcal strains throughout the 12-h dosing interval used in the study. Daptomycin and vancomycin were both active in vivo in these models of experimental enterococcal endocarditis caused by penicillin-resistant strains, irrespective of the mechanism of resistance. This activity correlated with the unique cell wall sites of action of these agents (binding to lipoteichoic acid and pentapeptide precursor, respectively) compared with the sites of action of beta-lactams (penicillin-binding proteins). Beta-Lactamase production by strain HH-22 precluded in vivo efficacy with ampicillin-gentamicin combinations. In contrast, this combination was active in vivo against strain SF-195, which exhibited intermediate-level penicillin resistance (MIC, 32 micrograms/ml), likely reflecting the ability of high-dose ampicillin to achieve enough binding to low-affinity penicillin-binding proteins to cause augmented aminoglycoside uptake.
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PMID:Comparison of daptomycin, vancomycin, and ampicillin-gentamicin for treatment of experimental endocarditis caused by penicillin-resistant enterococci. 132 32

Sixty-three cases of monomicrobial enterococcal infections treated with teicoplanin in two open clinical studies in Europe from 1982 to 1989 are presented. Infections were documented as endocarditis (n = 18); septicemia (n = 8); and urinary tract (n = 29), skin/soft-tissue (n = 6), or bone/joint (n = 2) infections. A total of 63 enterococcal strains were isolated; all of 29 strains tested were susceptible to teicoplanin (geometric mean MIC, 0.16 micrograms/mL; range, 0.06-0.5 micrograms/mL). Forty-eight patients were treated with teicoplanin alone and 15 were treated with teicoplanin in combination with an aminoglycoside. The rate of clinical cure was 84.1%; 4.8% of patients clinically improved, 7.9% had clinical recurrence, and 3.2% did not respond to therapy. Bacteriologic eradication was observed in 87.2% of patients; persistence, in 3.2%; recurrence, in 3.2%; and reinfection, in 4.8%. One case was not evaluable bacteriologically. Of 18 patients with endocarditis, 15 were cured with a mean daily dose of 5.4 mg/kg--six with monotherapy and nine with combination therapy. All patients with urinary tract infections were treated with monotherapy, and 89.7% were cured (mean daily dose, 4.6 mg/kg). Lower rates of clinical cure and bacteriologic eradication were observed in septicemic patients without endocarditis (62.5%). This study demonstrated a good efficacy of teicoplanin for the treatment of enterococcal infections due to susceptible strains, but further clinical studies would be useful for establishing optimal dosage and the indications for combination therapy, especially for severe infections.
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PMID:Efficacy of teicoplanin for enterococcal infections: 63 cases and review. 138 8

221 strains of Staphylococcus aureus oxacillin resistant (MetiR) caused nosocomial infections were isolated from 1985 to 1989 in a medical intensive care unit. The survey of susceptibility to antibiotics was established according to the computerized data of disk susceptibility test. The resistance phenotypes to beta-lactams, aminoglycosides and macrolides were established for epidemiological study. S. aureus infections were mainly bacteraemia (31%) and peritonitis (12%). These isolates were resistant to oxacillin with a high level (mean MIC 386 micrograms/ml). Their resistance phenotypes were MLSBc (constitutive resistance to macrolides, lincosamine and streptogramines B) in 53% and S + KGT (resistance to streptomycin, kanamycin, gentamicin and tobramycin) in 61%. All the isolates were susceptible to pristinamycin and vancomycin (MIC 0.1 and 2 micrograms/ml). These phenotypes related to the spread of multiply drug resistant strains were responsible of nosocomial outbreaks. Strains with the same pattern of resistance were isolated among the medical staff and in the environment. Infection control measures allowed to stop these outbreaks.
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PMID:[Staphylococcus aureus nosocomial infections in an intensive care milieu (1985-1989) in Tunis]. 144 73

Infection is the greatest problem in burn patients and topical antimicrobial agents must be chosen with great care, especially when cultured skin is grafted. We examined the cytotoxic effect of six antiseptics and six antibiotics commonly used on cultured human fibroblasts and keratinocytes. Cultured cells were exposed for 15 min to Hibitane (chlorhexidine), Biseptine (chlorhexidine+benzalkonium chloride+benzylic alcohol), Benzalkonium Chloride, Yellow Betadine (polyvidone-iodine+nonoxinol), Betadine Scrub (polyvidone-iodine+quaternary ammonium) and Green Betadine (polyvidone-iodine) and viability was determined using the MTT test. At therapeutic concentrations all the antiseptics are cytotoxic for fibroblasts and keratinocytes. Additionally the cells were exposed for 48 h to vancomycin, colistin, amikacin, imipeneme, pefloxaxin, piperacillin and cell viability was determined using the MTT test. The concentrations of antibiotics corresponding to the plasma peak obtained after therapeutic application were not cytotoxic to the tested cells. The CD50 was much higher than the MIC (from 125 to 875 times for keratinocytes and from 1400 to 5900 times for fibroblasts). These data suggest that commonly applied antiseptics must not be used before grafting cultured skin grafts. After grafting any infection can be controlled with topical applications of appropriate antibiotics.
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PMID:Cytotoxicity evaluation of antiseptics and antibiotics on cultured human fibroblasts and keratinocytes. 148 97

Strains of Escherichia coli (N = 124) and Proteus mirabilis (N = 29) harboring known beta-lactamases were analyzed as to their susceptibility to ampicillin, amoxicillin, and piperacillin alone and in combination with sulbactam, clavulanate, and tazobactam. With TEM 1-producing E. coli, a correlation between specific beta-lactamase activity and the MIC of piperacillin and ampicillin-sulbactam was observed. These strains also showed significant differences in susceptibilities to the various combinations, suggesting that, at least in strains resistant to one combination, several beta-lactam/beta-lactamase inhibitor combinations should be tested in the laboratory. All combinations tested enhanced the activity of the beta-lactam towards TEM 1-producing E. coli, piperacillin-tazobactam being the most active. The drugs were less active to OXA 1 enzymes; solely with piperacillin-tazobactam 90% of strains were within the therapeutic range of the drug. Sulbactam acted synergistically to chromosomally encoded beta-lactamases, whereas amoxicillin-clavulanate was inactive. Piperacillin and piperacillin-tazobactam inhibited all strains producing chromosomally encoded beta-lactamases at concentrations within the therapeutic range of the drugs. In contrast, TEM 2 of P. mirabilis was not sensitive to ampicillin-sulbactam, but to the other combinations; here again piperacillin-tazobactam was the most active.
Infection
PMID:Comparative in vitro activities of amoxicillin-clavulanate, ampicillin-sulbactam and piperacillin-tazobactam against strains of Escherichia coli and proteus mirabilis harbouring known beta-lactamases. 164 71

Between November 1988 and October 1989, 49 first-time pediatric liver transplant recipients at the Children's Hospital of Pittsburgh were prospectively monitored for the presence of stool colonization and the development of disease caused by vancomycin-resistant gram-positive cocci (VRGPC). Quantitative stool culturing was done on a weekly basis, and cultures were planted onto a selective medium for VRGPC. Isolates for which the MIC was greater than or equal to 8 were considered resistant to vancomycin. Patients were monitored clinically for the development of infection, and their charts were systematically reviewed for the use of antibiotics. Eighty-six isolates were recovered from 36 of the 49 patients. Enterococcal species were isolated from 31 patients and included Enterococcus gallinarum (n = 28), E. casseliflavus (n = 14), E. faecium (n = 9), E. faecalis (n = 2), E. mundtii (n = 2), and E. durans (n = 1). Stool colonization with vancomycin-resistant enterococci was noted to increase steadily during the first month after transplantation. Only 9 of 31 patients demonstrated clearance of these organisms in serial repeat cultures. Additional isolates of VRGPC included Lactobacillus confusus (n = 13), Lactobacillus spp. (n = 12), and Pediococcus pentosaceus (n = 4). Infection due to VRGPC developed in three patients: a urinary tract infection in two and peritonitis in one. E. faecium was the pathogen in each of these cases. The ranges of MICs of vancomycin were 8 to 32 micrograms/ml for all enterococcal isolates and greater than 128 micrograms/ml for Lactobacillus and Pediococcus isolates. All Lactobacillus and Pediococcus isolates were resistant to teicoplanin, although they were susceptible to daptomycin. All other isolates were susceptible to both teicoplanin and daptomycin. This study demonstrates that stool colonization with VRGPC may be a common and early finding among pediatric liver transplant recipients. However, infection appears to be uncommon.
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PMID:Recovery of vancomycin-resistant gram-positive cocci from pediatric liver transplant recipients. 177 55

320 recently isolated pathogens, 20 strains from each of 16 species, were investigated using Mueller-Hinton agar and DIN as well as NCCLS standards. The geometric mean of the agar dilution MICs of flomoxef were 0.44 mg/l for Staphylococcus aureus, 0.05 mg/l (Klebsiella oxytoca) to 12.6 mg/l (Enterobacter spp.) for enterobacteriaceae, 33.1 mg/l for Acinetobacter anitratus, 64 mg/l for Enterococcus faecalis, and more than 256 mg/l for Pseudomonas aeruginosa. For disk susceptibility testing of flomoxef a 30 micrograms disk loading and the following interpretation of inhibition zones using the DIN method were recommended: resistant-up to 22 mm (corresponding to MICs of 8 mg/l or more), moderately susceptible-23 to 29 mm (corresponding to MICs from 1 to 4 mg/l), and susceptible-30 mm or more (corresponding to MICs of 0.5 mg/l or less). The respective values for the NCCLS method using the American high MIC breakpoints are: resistant--up to 14 mm (corresponding to MICs of 32 mg/l or more), moderately susceptible--15 to 17 mm (corresponding to MICs of 16 mg/l), and susceptible--18 mm or more (corresponding to MICs of 8 mg/l or less).
Infection 1991
PMID:Interpretive criteria of antimicrobial disk susceptibility tests with flomoxef. 178 42

Cefpodoxime, the deesterified part of the orally available cefpodoxime proxetil, is active against most Enterobacteriaceae with MIC50 of 0.06 to 2 mg/l. Only Enterobacter cloacae and Citrobacter freundii strains show MIC50 of 4 mg/l. Coagulase negative staphylococci have a MIC50 of 2, while Staphylococcus aureus strains have a MIC of 4 mg/l. In comparison to other orally available cephalosporins cefpodoxime is slightly less active than cefixime and cefotiam against gram-negative bacteria but more active than cefuroxime, cefaclor, and cephalexin. Against staphylococci the activity of cefpodoxime is comparable to that of cefotiam and cefuroxime and superior to cefaclor and cephalexin, while cefixime does not have sufficient activity against these species. Like all cephalosporins cefpodoxime has no activity against enterococci.
Infection
PMID:In vitro activity of cefpodoxime and ten other cephalosporins against gram-positive cocci, Enterobacteriaceae and Pseudomonas aeruginosa, including beta-lactamase producers. 180 Mar 78

The interpretation of disk susceptibility testing with 30 micrograms cefpodoxime disks was evaluated on the basis of regression line analyses and preliminary MIC breakpoints of 2 and 4 mg/l. Using the DIN-58940 method, zone diameters up to 23 mm are resistant, 24 to 26 mm moderately susceptible, and 27 mm or more susceptible. The respective data for the NCCLS method are: up to 21 mm, 22 to 23 mm, and 24 mm or more.
Infection
PMID:Interpretive criteria of antimicrobial disk susceptibility tests with cefpodoxime. 180 Mar 81

The combined activities of trospectomycin, a spectinomycin analogue, and colloidal bismuth subcitrate against Helicobacter pylori were investigated, the agar dilution method being employed. Forty-seven strains of H. pylori were examined. An additive effect was observed in 89%, and a synergistic interaction in 11% of the isolates. There was no antagonism observed. The MIC50 of trospectomycin against H. pylori was 2 mg/l; the MIC ranged from 0.5 to 4 mg/l.
Infection
PMID:Combined activity of trospectomycin and colloidal bismuth subcitrate against Helicobacter pylori in vitro. 183 17


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