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Biomedical subjects

A A Medeiros

Publications and source records attributed to A A Medeiros.

At least 19 recordsLinked to original sources
PubMed1996

Predictors of effect of ampicillin-sulbactam against TEM-1 beta-lactamase-producing Escherichia coli in an in vitro dynamic model: enzyme activity versus MIC.

The clinical outcome in patients treated with ampicillin-sulbactam may not always be predictable by disc susceptibility testing or with the MIC as determined with a constant level (4 micrograms/ml) of the beta-lactamase inhibitor (MIC1). The enzyme activities (EA) and the MICs estimated at a constant ratio of ampicillin to sulbactam of 2:1 (MIC2) for 15 TEM-1 beta-lactamase-producing strains of Escherichia coli were examined as alternatives to MIC1 as predictors of the antibacterial effects of this combined drug as studied in an in vitro model which simulates ampicillin-sulbactam pharmacokinetic profiles observed in human peripheral tissues. Integral parameters describing the area under the bacterial count-time curve (AUBC), the area between the normal growth curve, and the killing curve of bacteria exposed to antibiotic (ABBC), and the second parameter expressed as a percentage of its maximal hypothetical value (ABBC/ABBCmax) were calculated. All three parameters correlated well with EA (AUBC, r = 0.93; ABBC, r = -0.88; ABBC/ABBCmax, r = -0.91) and with MIC2 (r = 0.94, -0.94, and -0.95, respectively) but not with MIC1. Both EA and MIC2 can be considered reliable predictors of the antibacterial effect of ampicillin-sulbactam in an in vitro model. These correlations suggest that in vitro kinetic-dynamic models might be useful to reexamine established susceptibility breakpoints obtained with data based on the MIC1 (MICs obtained with constant levels of beta-lactamase inhibitors). These data also suggest that quantitative determinations of bacterial beta-lactamase production and MICs based on the component concentration ratio observed in vivo might be useful predictors of the effect of ampicillin-sulbactam and other beta-lactam-inhibitor combinations.

Ampicillin↗
PubMed1996

Characterization of IMI-1 beta-lactamase, a class A carbapenem-hydrolyzing enzyme from Enterobacter cloacae.

In 1984, a year prior to the U.S. approval of imipenem for clinical use, a wound isolate and a bile isolate of Enterobacter cloacae were obtained from two patients in a California hospital. These isolates were resistant to imipenem, penicillins, and inhibitor combinations; early cephalosporins such as cephalothin, cefamandole, and cefoxitin; and cefoperazone. However, they were susceptible (MICs, < 4 micrograms/ml) to cefotaxime, ceftriaxone, ceftazidime, and moxalactam. Both strains produced an apparent TEM-1 beta-lactamase; an inducible NmcA-type imipenem-hydrolyzing beta-lactamase, IMI-1, with a pl of 7.05; and an inducible beta-lactamase with a pI of 8.1, typical of an E. cloacae AmpC beta-lactamase. Purified IMI-1 hydrolyzed imipenem and benzylpenicillin at modest rates, but more slowly than cephaloridine. The enzyme was inhibited by clavulanic acid and tazobactam. EDTA did not inhibit the cephaloridine-hydrolyzing activity. The beta-lactamase gene encoding IMI-1, imiA1, was cloned from E. cloacae 1413B. Sequence analysis identified the imiA1 gene as encoding a class A serine beta-lactamase. Both the imiA1 DNA and encoded amino acid sequences shared greater than 95% identity with the NmcA gene and its encoded protein. DNA sequence analysis also identified a gene upstream of imiA1 that shares > 95% identity with nmcR and that may encode a regulatory protein. In conclusion, IMI-1, a carbapenem-hydrolyzing beta-lactamase inhibited by clavulanic acid, was identified as a group 2f, class A, carbapenem-hydrolyzing cephalosporinase.

Amino Acid Sequence↗
PubMed1995

The growing threat of antibiotic-resistant Streptococcus pneumoniae.

Resistance to penicillin has spread worldwide during the past 25 years. Strains resistant to alternative antibiotics have also emerged. Strains resistant to multiple antibiotics increasingly are isolated worldwide. Recently, isolates of penicillin-resistant S. pneumoniae resistant to cefotaxime and ceftriaxone have caused meningitis. As a result, recommendations for the empiric therapy of pneumococcal infections, especially meningitis, are changing.

Bacterial Vaccines↗
PubMed1995

Controlling vancomycin-resistant enterococci.

After controlling an epidemic of vanB-type vancomycin-resistant Enterococcus faecium (VRE), we contained a subsequent vanA E faecium outbreak by using prospective laboratory-based surveillance, placing patients with VRE in private rooms, requiring the use of both gowns and gloves by all personnel entering the patients' rooms, and conducting prevalence surveys of patients on affected wards.

Anti-Bacterial Agents↗
PubMed1994

IS6770, an enterococcal insertion-like sequence useful for determining the clonal relationship of clinical enterococcal isolates.

Enterococci expressing resistance to antimicrobial agents are increasingly important nosocomial pathogens. Effective strategies to prevent or abort outbreaks of resistant enterococcal infection will rely on an accurate understanding of the mechanisms by which these organisms spread. A 1065-bp insertion-like sequence (IS6770) is present in varying copy numbers in > 90% of enterococcal strains thus far examined. Hybridization patterns resulting from hybridization of enterococcal genomic DNA with an internal IS6770 probe vary considerably between unrelated strains and correlate well with results of pulsed-field gel electrophoresis and field-inversion gel electrophoresis in identifying clonal relationships among enterococcal isolates. IS6770 analysis of several outbreaks of resistant enterococci has confirmed the spread of single resistant clones rather than the emergence of resistance within the resident flora. These results suggest that IS6770 hybridization will be a useful tool for tracing the epidemiology of nosocomial enterococcal infections.

Amino Acid Sequence↗
PubMed1994

Pharmacodynamics of piperacillin alone and in combination with tazobactam against piperacillin-resistant and -susceptible organisms in an in vitro model of infection.

The pharmacodynamics of dosage regimens of piperacillin alone or in combination with tazobactam against piperacillin-resistant or -susceptible bacteria were studied in an in vitro model of infection. Experiments were conducted by using a fixed daily exposure of 12 g of piperacillin, given as 3 g alone or in combination with tazobactam at 0.375 g every 6 h, or the same total dose of the combination given as 4 g of piperacillin plus 0.5 g of tazobactam every 8 h. The addition of tazobactam to piperacillin, irrespective of the dosing interval, did not alter the killing of piperacillin-susceptible organisms (Escherichia coli J53 and Pseudomonas aeruginosa ATCC 27853). In contrast, experiments with an isogenic TEM-3-containing transconjugant of E. coli J53 (E. coli J53.2-TEM-3) that was resistant to piperacillin (MIC, 128 micrograms/ml) showed that the addition of tazobactam resulted in bacterial killing similar to that observed with the wild-type strain. Although tazobactam concentrations fell to less than 4 mg/liter (the concentration associated with a reduction in the piperacillin MIC from 128 to 2 mg/liter) 2 to 3 h after a dose, a similar degree of bacterial killing was observed when the same total 24-h dose of piperacillin-tazobactam was fractionated into dosing intervals of every 6 or 8 h. Investigations with Staphylococcus aureus 7176 (piperacillin MIC, 128 micrograms/ml) showed that the addition of tazobactam, again irrespective of dosing interval, also resulted in net bacterial killing which was not seen with piperacillin alone. These data support the use of extended dosing intervals (every 8 h) of piperacillin-tazobactam in the treatment of infections caused by piperacillin-resistant bacteria.

Bacteria↗
PubMed1994

Outbreak of multidrug-resistant Enterococcus faecium with transferable vanB class vancomycin resistance.

Enterococcus faecium strains resistant to ampicillin, high levels of gentamicin, and vancomycin but susceptible to teicoplanin (vanB class vancomycin resistance) were recovered from 37 patients during an outbreak involving a 250-bed university-affiliated hospital. Three isolates with vancomycin MICs ranging from 8 to 256 micrograms/ml all hybridized with a vanB probe. Restriction endonuclease analysis of chromosomal and plasmid DNA suggested that all isolates tested were derived from a single clone. Vancomycin resistance was shown to be transferable. Risk factors for acquiring the epidemic strain included proximity to another case patient (P, 0.0005) and exposure to a nurse who cared for another case patient (P, 0.007). Contamination of the environment by the epidemic strain occurred significantly more often when case patients had diarrhea (P, 0.001). Placing patients in private rooms and requiring the use of gowns as well as gloves by personnel controlled the outbreak. These findings suggest that multidrug-resistant E. faecium strains with transferable vanB class vancomycin resistance will emerge as important nosocomial pathogens. Because extensive environmental contamination may occur when affected patients develop diarrhea, barrier precautions, including the use of both gowns and gloves, should be implemented as soon as these pathogens are encountered.

Adult↗
PubMed1993

Spread of methicillin-resistant Staphylococcus aureus in a hospital after exposure to a health care worker with chronic sinusitis.

A dramatic increase in the incidence of methicillin-resistant Staphylococcus aureus at a teaching hospital was documented to be due to three factors: a hospital-wide outbreak of 32 cases caused by an epidemic strain, an increase in the number of nosocomial cases caused by several other strains, and an increase in the number of patients admitted carrying strains acquired at other institutions. Case patients with the epidemic strain were significantly more likely than control patients to have had previous exposure to a respiratory therapist (P = .005) who had chronic sinusitis due to the epidemic strain. The plasmid DNA of isolates from the implicated respiratory therapist and affected patients yielded the same patterns on restriction endonuclease digestion. Implementation of general control measures and eradication of the respiratory therapist's sinusitis and nasal carriage terminated the epidemic. Establishing the importance of the infected health care worker by epidemiological methods led to control of the outbreak without the institution of wide-scale culture of specimens from personnel and the environment or other expensive and labor-intensive measures.

Aged↗
PubMed1993

High rate of erythromycin and clarithromycin resistance among Streptococcus pneumoniae isolates from blood cultures from Providence, R.I.

Four (5%) of 81 recent isolates of Streptococcus pneumoniae from the blood of adult patients but no isolates from pediatric patients (n = 51) were resistant (MIC, > or = 1 microgram/ml) to erythromycin. The MICs of clarithromycin were slightly lower than those of erythromycin, but there was complete cross-resistance. Routine testing and surveillance are needed to determine whether erythromycin resistance among S. pneumoniae isolates is increasing throughout the United States.

Adult↗
PubMed1992

Emergence and nosocomial transmission of ampicillin-resistant enterococci.

Between 1986 and 1988, the incidence of ampicillin-resistant enterococci increased sevenfold at a university-affiliated hospital. Forty-three patients acquired nosocomial infections with ampicillin-resistant enterococci, most of which were also resistant to mezlocillin, piperacillin, and imipenem. An analysis of plasmid and chromosomal DNAs of isolates revealed that the increase was due to an epidemic of 19 nosocomial infections that yielded closely related strains of Enterococcus faecium and to a significant increase in the incidence of nonepidemic, largely unrelated strains of ampicillin-resistant enterococci. The nonepidemic strains were identified as E. faecium, E. raffinosus, E. durans, and E. gallinarum. A logistic regression analysis revealed that patients with nonepidemic resistant strains were 16 times more likely than controls to have received preceding therapy with imipenem. In our institution, the increase in the incidence of ampicillin-resistant enterococci appears to be due to the selection of various strains of resistant enterococci by the use of imipenem and to the nosocomial transmission of E. faecium and E. raffinosus.

Adult↗
PubMed1991

Molecular distribution of ROB-1 beta-lactamase in Actinobacillus pleuropneumoniae.

The plasmid content and molecular distribution of the ROB-1 beta-lactamase was investigated in 31 swine isolates of Actinobacillus pleuropneumoniae. Three types of plasmid patterns were observed in ampicillin-resistant isolates: a predominant one consisting of 2.6-, 2.9-, and 5.0-kb plasmids and two other patterns consisting of 4.2- and 5.5-kb plasmids and of a 6.8-kb plasmid. Plasmid DNA preparations were hybridized with a blaROB-1 intragenic fragment from the Haemophilus influenzae Rrob plasmid. Positive hybridizations were observed with all ampicillin-resistant isolates. The blaROB-1 gene was found on 3 plasmids of 2.6, 5.5, and 6.8 kb. One swine isolate of Pasteurella multocida also had a 2.6-kb plasmid bearing blaROB-1. ROB-1 was confirmed in typical isolates by isoelectric focusing and blaROB-1 sequences were confirmed by polymerase chain reaction amplification with an intragenic set of primers. Plasmids bearing blaROB-1 were successfully electro-transformed in a susceptible A. pleuropneumoniae isolate. These results emphasize the importance of ROB-1 in A. pleuropneumoniae and identify a possible reservoir of beta-lactam resistance.

Actinobacillus↗
PubMed1991

Failure of routine susceptibility tests to detect imipenem resistance among strains of methicillin-resistant Staphylococcus aureus.

We tested 75 methicillin-resistant Staphylococcus aureus strains for susceptibility to imipenem by using disk diffusion tests and broth microdilution tests with standard and heavy inocula. Population analysis was performed on isolates that appeared to be susceptible by these methods. All of the strains contained subpopulations of cells that are phenotypically resistant to imipenem.

Drug Resistance, Microbial↗
PubMed1990

A common-source outbreak of Staphylococcus epidermidis infections among patients undergoing cardiac surgery.

A single strain of Staphylococcus epidermidis caused an outbreak of postoperative wound infections and endocarditis during a 6-month period. Infections caused by the epidemic strain developed more frequently in valve surgery patients than in those undergoing coronary artery bypass graft surgery (P = .03) and occurred only in patients operated on by surgeon A. None of 17 members of the cardiac surgery team carried the epidemic strain in their anterior nares, axillae, or inguinal folds. Hand cultures were performed on 8 surgical personnel, and only surgeon A carried the epidemic strain on his hands. Isolates from cardiac surgery patients, bypass pump blood cultures, and the hands of the implicated surgeon all had identical antimicrobial susceptibility patterns, plasmid profiles, and EcoRI restriction endonuclease digest patterns. In the 24 months after control measures were implemented, no infections caused by the epidemic strain occurred among open heart surgery patients. The findings suggest that the common-source outbreak of infections among cardiac surgery patients was due to carriage of a strain S. epidermidis on the hands of a cardiac surgeon.

Adult↗
PubMed1990

Induction of beta-lactamase and methicillin resistance in unusual strains of methicillin-resistant Staphylococcus aureus.

Two unusual, heterogeneously-resistant, strains of Staphylococcus aureus appeared resistant to oxacillin, but susceptible to methicillin by disc diffusion methods. In agar dilution tests, both strains were oxacillin-resistant. One was susceptible to methicillin, and the other gave a paradoxical reaction, with growth only on plates containing low (0.5, 1 and 2 mg/l) and high (32 and 64 mg/l) concentrations of antibiotic. Induction of methicillin resistance was tested by inoculating each strain on to agar plates containing an inhibitory concentration of methicillin (8 mg/l), and then placing discs containing inducers (oxacillin, nafcillin, methicillin and CBAP [2-(2'-carboxyphenyl) benzoyl-6-aminopenicillanic acid]) on the agar surface. Colonies grew only around discs containing effective inducers. Oxacillin and CBAP were much more potent inducers of methicillin resistance and beta-lactamase than was nafcillin or methicillin. These data suggest that the mechanism that regulates induction of the low-affinity penicillin binding protein (PBP-2') may be altered in these strains. Similar mechanisms appear to induce both beta-lactamase and methicillin resistance.

Bacterial Proteins↗