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Biomedical subjects

H C Neu

Publications and source records attributed to H C Neu.

At least 505 records · Page 28Linked to original sources
PubMedDate not supplied

Resistance of Xanthomonas maltophilia to antibiotics and the effect of beta-lactamase inhibitors.

We examined the susceptibility of 50 isolates of Xanthomonas maltophilia and the effect of beta-lactamase inhibitors upon the susceptibility. The majority of isolates were resistant to azlocillin, piperacillin, mezlocillin, ticarcillin, cefotaxime, ceftizoxime, ceftriaxone, cefoperazone, and ceftazidime. All isolates were resistant to imipenem, CGP 31608, aztreonam, and carumonam. Although disk susceptibility tests showed that the combination of clavulanate with ticarcillin inhibited many isolates, at a ratio of 1:20 few isolates were susceptible to the combination. Addition of clavulanate to aztreonam and to imipenem failed to make organisms susceptible. Sulbactam combined with cefoperazone made some organisms susceptible, but ampicillin-sulbactam was ineffective, whereas tazobactam combined with piperacillin at a ratio of 1:4 made half the isolates have MICs of 32 micrograms/ml or less. The beta-lactamases from the isolates hydrolyzed all of the beta-lactams.

Anti-Bacterial Agents↗
PubMedDate not supplied

Synergy of new C-3 substituted cephalosporins and tobramycin against Pseudomonas aeruginosa and Pseudomonas cepacia.

The effects of the combination of E-1040, a new cephalosporin, ceftazidime, cefpirome, or cefepime with tobramycin against 40 Pseudomonas aeruginosa and 16 P. cepacia isolates from cystic fibrosis patients were examined. Synergy fractional inhibitory concentration less than or equal to 0.5 was found against P. aeruginosa when tobramycin was combined with E-1040 32%, cefpirome 32%, cefepime 22%, and ceftazidime 22%. Fifty-two percent of isolates showed an additive response for E-1040, 60% for cefpirome, 45% cefepime, and 55% ceftazidime, p greater than 0.05. The differences were not statistically significant. Synergy was not more likely to be achieved if the isolates were susceptible or resistant to either the aminoglycoside or cephalosporin. None of the E-1040-resistant isolates, all of which were tobramycin-resistant, became susceptible when tested with an aminoglycoside, whereas 15 of 34 cefpirome-resistant, 13 of 30 cefepime-resistant, and seven of 14 ceftazidime-resistant isolates became susceptible. Synergy of aminoglycoside and the cephalosporins against P. cepacia was found for 25% with E-1040, 44% with cefpirome, 38% with cefepime, and 31% with ceftazidime. These differences were not statistically significant.

Cephalosporins↗
PubMedDate not supplied

Antibacterial activity and beta-lactamase stability of MDL 19,592, an oral cephalosporin.

We compared the in vitro activity and beta-lactamase stability of MDL 19,592, an orally absorbed cephalosporin, with that of cephalexin and cefaclor. It inhabited Staphylococcus aureus at less than or equal to 4 micrograms/ml, Streptococcus pyogenes at 0.25 microgram/ml, sero groups B, C and G streptococci at 1 microgram/ml, and Streptococcus pneumoniae at 2 micrograms/ml. It was slightly more active than cefaclor and cephalexin. MDL 19,592 did not significantly inhibit Enterobacteriaceae, enterococci, Listeria monocytogenes, Pseudomonas aeruginosa, and Acinetobacter spp. strains (MIC greater than or equal to 32 micrograms/ml). MDL 19,592 was not hydrolyzed by the plasmid beta-lactamases TEM-1 and SHV-1 of Klebsiella but was hydrolyzed by the TEM-3, Staphylococcus aureus beta-lactamase, and the chromosomal-mediated Enterobacter cloacae P99 enzymes.

Bacteria↗
PubMedDate not supplied

Overview of mechanisms of bacterial resistance.

Many antimicrobial agents have been either found in nature or synthesized in the past 45 years. Antibacterial agents inhibit cell-wall formation, disrupt cytoplasmic membrane function, prevent DNA synthesis, interfere with protein synthesis, and halt folate synthesis. Resistance to antibiotics is a result of three major mechanisms: prevention of the antibacterial agent from reaching its receptor site, production of altered targets, and destruction or modification of the agents. Bacterial resistance has occurred due to chromosomal changes or the presence of plasmids and transposons. Resistance to beta-lactams is the result of beta-lactamases and the production of altered penicillin-binding proteins as well as altered cell-wall permeability. Important examples of these resistance forms occur in staphylococci and pneumococci which have altered penicillin-binding proteins. A new form of target change has been the production of proteins in enterococci that inhibit the activity of glycopeptides. Beta-lactamases are present in both Gram-positive and Gram-negative species; recently, new plasmid beta-lactamases have been isolated that destroy iminomethoxy and iminocarboxy cephalosporins. Resistance to aminoglycosides is due to enzymes that acetylate, adenylate, or phosphorylate aminoglycosides that inhibit binding to ribosomes and thus cause the poor uptake of drug. Tetracycline resistance is due to plasmids which cause efflux of the agent from the cytoplasm. Macrolide and lincinoid resistance is the result of an altered 23S ribosomal component of the 50S ribosomes. Sulfonamide and trimethoprim resistance is due to production of altered synthetase and reductase enzymes essential in the synthesis of folate.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗
PubMedDate not supplied

In vitro activity of CP-74,667. A new fluoroquinolone compared with other quinolones.

CP-74,667, a 6-fluoro-7-bridged piperazinyl-1-cyclopropyl-4 quinolone, inhibited 90% of staphylococci, beta-hemolytic streptococci, enterococci, Enterobacteriaceae, and Pseudomonas aeruginosa at less than or equal to 2 micrograms/ml. Ciprofloxacin-resistant, methicillin-resistant Staphylococcus aureus had minimum inhibitory concentration (MIC50) of 4 micrograms/ml and an MIC90 of 8 micrograms/ml. CP-74,667 was fourfold more active than ciprofloxacin against Streptococcus pneumoniae and St. pyogenes, but equal or less active than tosufloxacin against Gram-positive species. The MIC90 for P. aeruginosa was 5 micrograms/ml similar to temafloxacin. The CP-74,667 MIC90 for Bacteroides fragilis was 2 micrograms/ml, equal to tosufloxacin and temafloxacin. Activity was eight- to 16-fold less at pH 5.5 compared with pH 7.4 and also eight- to 16-fold less in urine. Magnesium ions markedly increased the CP-74,667 minimum bactericidal concentrations (MBCs). The development of resistance to CP-74,667 was similar to that found for other fluoroquinolones.

Anti-Infective Agents↗
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Activity of cephalosporins against coagulase-negative staphylococci.

Staphylococcus epidermidis has become an increasingly important pathogen as the cause of serious postoperative infection after heart and orthopedic surgery. We studied the susceptibilities of 80 blood, sternotomy, and hip isolates to vancomycin, cefazolin, cefuroxime, oxacillin, erythromycin, ciprofloxacin, and ofloxacin. The MIC90 of methicillin-susceptible isolates was 4 micrograms/ml for cefazolin and cefamandole, 8 micrograms/ml for cefuroxime, and 4 micrograms/ml for vancomycin. At 48 hr the MIC90 rose to 32 micrograms/ml for cefazolin and greater than 128 micrograms/ml for cefuroxime, and remained at 4 micrograms/ml for cefamandole and vancomycin. The MIC90 of methicillin-resistant isolates at 48 hr was 16 micrograms/ml cefamandole, 64 micrograms/ml cefazolin, greater than 128 micrograms/ml cefuroxime, and 4 micrograms/ml vancomycin. Ciprofloxacin and ofloxacin inhibited the majority of isolates at 1 microgram/ml, and vancomycin at 4 micrograms/ml. The new peptolide, daptomycin, also inhibited S. epidermidis at less than or equal to 1 microgram/ml.

Cefamandole↗
PubMedDate not supplied

Direct detection and amplification of Helicobacter pylori ribosomal 16S gene segments from gastric endoscopic biopsies.

Helicobacter pylori is an organism thought to play an important causative role in gastritis and peptic ulcer diseases. We have designed an RNA dot blot assay for the detection of H. pylori, using as probe a synthetic oligonucleotide complementary to its 16S rRNA. We have also used oligonucleotide primers, complementary to conserved sequences within bacterial ribosomal 16S genes, to amplify a H. pylori ribosomal 16S DNA fragment via the polymerase chain reaction (PCR). After determining the DNA sequence of this amplified H. pylori fragment, primers were designed for specific PCR amplification of H. pylori ribosomal 16S DNA sequences. Samples from clinical endoscopic biopsies were PCR amplified with universal 16S ribosomal primers to detect the presence of bacteria and with H. pylori-specific primers to uniquely detect H. pylori. Finally, by comparing the H. pylori-specific PCR assay to commonly used diagnostic tests, we demonstrate that the molecular technique of PCR amplification shows promising applications for the clinical detection of H. pylori.

Base Sequence↗
PubMedDate not supplied

In vitro activity of HRE 664, a penem antibiotic.

HRE 664, a new penem antibiotic, inhibited 90% of Escherichia coli, Klebsiella, Citrobacter diversus, Proteus mirabilis, Proteus vulgaris, Salmonella, Shigella, Providencia, Aeromonas, and Morganella at less than or equal to 2 micrograms/ml but was considerably less active than cefotaxime, ceftazidime, and imipenem. It did not inhibit Pseudomonas aeruginosa (MIC greater than 128 micrograms/ml). HRE 664 inhibited Enterobacter spp., Citrobacter freundii, and Serratia marcescens at 1-8 micrograms/ml, two- to fourfold higher MICs than imipenem. HRE 664 inhibited methicillin-susceptible Staphylococcus aureus and Staphylococcus epidermidis at less than or equal to 0.12 micrograms/ml, but methicillin-resistant S. aureus and S. epidermidis were resistant. Group A, C, and G streptococci and Streptococcus pneumoniae were inhibited by 0.06 micrograms/ml. Bacteroides and Clostridium species were inhibited by 0.25 micrograms/ml comparable to imipenem. HRE 664 was not hydrolyzed by beta-lactamases TEM-1, TEM-2, TEM-3, TEM-5, SHV-1, PSE-1, PSE-4, OXA-2, OXA-3, K-1, P99, Morganella, P. vulgaris, and S. aureus PC-1 but was hydrolyzed by the beta-lactamase of Xanthomonas maltophilia.

Amikacin↗
PubMedDate not supplied

Antibacterial activity of rokitamycin compared with that of other macrolides.

The activity of rokitamycin, a 16-membered macrolide, was compared with other macrolides and agents used to treat respiratory infections. Rokitamycin had in vitro activity against streptococci and Streptococcus pneumoniae comparable to the other macrolides, inhibiting most organisms at less than 0.03 to 0.5 microgram/ml. It was the most active macrolide agent against Staphylococcus aureus, inhibiting 90% at 1 microgram/ml. Macrolide-resistant streptococci and staphylococci in which resistance was inducible were inhibited, but constitutively resistant Gram-positive bacteria were resistant. Rokitamycin was less active than erythromycin against Haemophilus influenzae, but had activity comparable to erythromycin against Moraxella catarrhalis and Neisseria gonorrhoeae. It inhibited Clostridium spp. and peptostreptococci, but had poor activity against Bacteroides species. Rokitamycin was bactericidal for streptococci and staphylococci, but not for enterococci. Overall rokitamycin has in vitro activity comparable to currently available 14-membered macrolides. Its clinical utility will be influenced by the degree of metabolism to less active metabolites since 70% is rapidly metabolized.

Anti-Bacterial Agents↗
PubMedDate not supplied

In vitro activity of an oxycephem OCP 9-176 compared with its sulfur analog and other beta-lactams.

OCP 9-176 is an oxycephem antibiotic that contains a 2-aminothiazolyl, carboxypropyl side chain at C-7 and a pyridinium thiomethyl group at C-3. OCP 9-176 was generally twofold less active than its sulfur-containing analog ME 1228 against Escherichia coli, Klebsiella pneumoniae, Klebsiella oxytoca, Providencia stuartii, Proteus vulgaris, and Serratia marcescens. Activity against Enterobacter cloacae and Citrobacter freundii was equivalent. OCP 9-176 was twofold less active than ME-1228 against Pseudomonas aeruginosa and Acinetobacter species. Activity of the two agents was similar against Staphylococcus aureus and Staphylococcus epidermidis. Although OCP 9-176 inhibited E. coli containing TEM-1 and TEM-2, it was less active than ME-1228. Klebsiella organisms with SHV-1 and K-2 beta-lactamases were inhibited, but TEM-3-containing isolates had MICs of 16 micrograms/ml. OCP 9-176 was minimally hydrolyzed by TEM-1, PSE-1, K-1, and P99, and it was a poor inhibitor of P99. Replacement of sulfur with oxygen does not increase the activity of compounds with sulfopyridinium methyl groups at C-3.

Anti-Bacterial Agents↗
PubMedDate not supplied

In vitro activity of LY264826 compared to other glycopeptides and daptomycin.

LY264826 a new naturally occurring glycopeptide inhibited 90% of methicillin-susceptible and -resistant Staphylococcus aureus at 1 micrograms/ml. LY264826 had similar activity against methicillin-susceptible and -resistant coagulase-negative staphylococci. The LY264826 MIC90 for Streptococcus pyogenes was 0.25 microgram/ml, twofold more active than vancomycin and twofold less active than teicoplanin. LY264826 was eightfold more active than vancomycin and twofold more active than teicoplanin against enterococci. LY264826 inhibited Streptococcus pneumoniae at 0.25 microgram/ml and Listeria monocytogenes at 0.5 microgram/ml. Clostridium were inhibited by less than or equal to 0.25 microgram/ml of LY264826 and peptococci, peptostreptococci, and Fusobacterium were inhibited by less than 0.5 microgram/ml. Bacteroides species were LY284826 -resistant as were all Enterobacteriaceae, Flavobacterium, and Neisseria spp. Minimum bactericidal and inhibitory concentrations (MBCs and MICs) were within a dilution for S. aureus, S. pyogenes, and S. pneumoniae, but greater than or equal to 32-fold greater for enterococci.

Anti-Bacterial Agents↗
PubMedDate not supplied

In vitro activity of a new cephalosporin ME-1206 compared with other agents.

The in vitro activity of ME-1206, a new aminothiazolyl cephalosporin that can be orally absorbed when converted to an ester, was compared with that of other beta-lactams. ME-1206 inhibited 50% of the Enterobacteriaceae at 2 micrograms/ml, similar to cefotaxime, ceftazidime, and cefixime. It did not inhibit, MIC greater than or equal to 32 micrograms/ml, Enterobacter species or Citrobacter freundii resistant to cefotaxime and ceftazidime, and it was less active than cefotaxime and ceftazidime against Serratia marcescens. Haemophilus influenzae, Neisseria gonorrhoeae, and Moraxella catarrhalis were inhibited by less than or equal to 0.25 micrograms/ml of ME-1206 inhibited hemolytic streptococci groups A, B, C, and G, MIC90 0.06 micrograms/ml, but it did not inhibit enterococci. Pseudomonas aeruginosa and other pseudomonads were resistant to ME-1206. MICs and MBCs of ME-1206 for susceptible species were within a dilution. ME-1206 was not hydrolyzed by TEM-1 or TEM-2, but was hydrolyzed by TEM-3 and TEM-5. ME-1206 was hydrolyzed by beta-lactamases of Morganella, Proteus vulgaris, and K1 of Klebsiella oxytoca, but minimally by the P99 beta-lactamase of Enterobacter cloacae. ME-1206 is comparable in in vitro activity and beta-lactamase stability to many of the current cephalosporins.

Amikacin↗
PubMedDate not supplied

Oral ofloxacin therapy of infections due to multiply-resistant bacteria.

We determined the efficacy and safety of orally administered ofloxacin, 400 mg twice daily, in the treatment of infections due to multiply-resistant bacteria. Patients (n = 99) were treated for 84 infections in 82 patients evaluable for efficacy with a bacteriologic response of 71%. Organisms treated included Pseudomonas aeruginosa (39), Staphylococcus aureus (11), Serratia marcescens (9), Enterobacter species (7), five each of Escherichia coli, Citrobacter, Salmonella, Klebsiella, and other organisms. The overall clinical responses was 89%: 28 (90%) of 16 osteomyelitis, 10 (83%) of 12 urinary tract infections, and three of three bacteremias. Insomnia occurred in 27% and responded to dose reduction. Resistance of P. aeruginosa to ofloxacin developed in 15% of isolates. No hepatic, renal, or hematologic toxicity developed in spite of long therapy, 283 days. Ofloxacin was an effective therapy for lower respiratory, urinary, bone, and soft tissue infections due to multiply-resistant Gram-negative bacteria and is effective for selected Staphylococcus aureus infections.

Administration, Oral↗
PubMedDate not supplied

Fleroxacin combined with rifampin.

We determined the effect of the combination of rifampin and fleroxacin against Enterobacteriaceae and streptococcal species. None of the 65 isolates tested by checkerboard assay demonstrated synergy, 12% of isolates showed an additive effect; 86.7% were indifferent, and only 1 isolate showed antagonism. The mean FIC was 1.2. When using 2 and 8 micrograms/ml of rifampin, fleroxacin MICs of 285 isolates of Enterobacteriaceae, Pseudomonas aeruginosa, Haemophilus influenzae, staphylococci, streptococci, Bacteroides, and Clostridium were not increased, but synergy was not demonstrated. Time-kill studies against Escherichia coli, P. aeruginosa, Enterobacter cloacae, Staphylococcus aureus, and Enterococcus faecalis failed to show increased killing when the two agents were present at one-half the MBC. The fleroxacin-rifampin interaction is one of indifference but provides coverage for species not adequately inhibited by fleroxacin.

Acinetobacter↗
PubMedDate not supplied

Antimicrobial effects of the combination of ceftibuten and an orally absorbed penem SCH 29482.

Ceftibuten is a new beta-lactamase-stable 3-aminothiazolyl cephalosporin that lacks activity against staphylococci and group-B streptococci. We determined the effect of the combination of ceftibuten with SCH 29482, an orally absorbed penem. The combination of the two agents was additive for 25% or indifferent for 57% of the Gram-positive species, Haemophilus, and Moraxella tested with a mean fractional inhibitory concentration (FIC) index of 0.75. The combination of ceftibuten and SCH 29482 was also indifferent for Bacteroides fragilis and other Bacteroides species, all of which were inhibited by less than or equal to micrograms/ml of SCH 29482. Antagonism of the combination was found for 80% of Serratia marcescens and for 30% of Citrobacter freundii and Enterobacter cloacae. Overall, the combination of ceftibuten and SCH 29482 at concentrations that can be achieved in serum after ingestion of 400 and 50 micrograms/ml, respectively, provided antibacterial activity against most Gram-positive aerobic and anaerobic species that cause upper respiratory, intraabdominal, and urinary infections.

Anti-Bacterial Agents↗
PubMedDate not supplied

In vitro activity of cefquinome, a new cephalosporin, compared with other cephalosporin antibiotics.

The in vitro activity of cefquinome, a new aminothiazolyl cephalosporin with a C-3 bicyclic pyridinium group, was compared with ceftazidime, cefpirome, and cefepime. Cefquinome inhibited members of the Enterobacteriaceae at less than or equal to 0.5 microgram/ml for Escherichia coli, Klebsiella pneumoniae, K. oxytoca, Citrobacter diversus, Salmonella Shigella, Proteus mirabilis, Morganella, and Providencia. Although most Citrobacter freundii and Enterobacter cloacae were inhibited by less than 2 micrograms/ml, some strains resistant to ceftazidime were resistant, [minimum inhibitory concentration (MIC) greater than 16 micrograms/ml]. Serratia marcescens were inhibited by less than 1 microgram/ml and Pseudomonas aeruginosa by 8 micrograms/ml similar to the activity of cefepime. The majority of Haemophilus influenzae and Neisseria gonorrhoeae were inhibited by less than 0.25 microgram/ml. Most enterococci had cefquinome MICs of 4-8 micrograms/ml. Cefquinome was extremely active against group-A streptococci and Streptococcus pneumoniae with MICs less than 0.12 microgram/ml. 90% of methicillin-susceptible Staphylococcus aureus 90% were inhibited by 2 micrograms/ml. Overall, the in vitro activity of cefquinome was comparable with aminothiazolyl cephalosporins. It inhibited some Enterobacter and Citrobacter freundii resistant to ceftazidime as did cefpirome and cefepime. Cefquinome was not destroyed by the common plasmid beta-lactamases TEM-1, TEM-2, SHV-1, or by the chromosomal beta-lactamases of Klebsiella, Branhamella, and Pseudomonas, but it was hydrolyzed by TEM-3, TEM-5, and TEM-9. Its activity was not adversely decreased in different medium or protein, and minimum bactericidal concentrations (MBCs) for most species except for Enterobacter were within a dilution of MICs.

Bacteria↗