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H C Neu

Publications and source records attributed to H C Neu.

At least 271 records · Page 15Linked to original sources

Carbenicillin and ticarcillin.

Carbenicillin and ticarcillin are penicillins which were initially developed as agents to treat serious Pseudomonas infections in the seriously ill hospitalized patient. These drugs have made a major contribution to improved survival in the neutropenic patients with Pseudomonas infection, the burn patient and to the care of the patient with cystic fibrosis. Areas of use for the compounds have enlarged to include aspiration pneumonitis in hospitalized patients, intra-abdominal and pelvic sepsis, and infections due to Proteus and Enterobacter species. Careful attention to the pharmacology of the agents is necessary to achieve clinical and bacteriologic success and to avoid the toxic side-effects such as bleeding and hypokalemia associated with the use of these agents. A decade of use has shown that the agents have remained effective agents in institutions in which their use has not been abused. It is too early to clearly position azlocillin, mezlocillin, and piperacillin. In the next few years the role of these potent compounds will be established. As noted in this review, these three agents have been used with success to treat all of the aforementioned infections. With these drugs it is also essential that the physician closely correlate in vitro data and the human pharmacology of the drugs if he or she wishes to achieve the most effective response from the agents.

Anaerobiosis↗

Antibacterial activity and beta-lactamase stability of ceftazidime, an aminothiazolyl cephalosporin potentially active against Pseudomonas aeruginosa.

The in vitro activity and beta-lactamase stability of ceftazidime were evaluated against 700 gram-positive and gram-negative bacteria. Ceftazidime was less active than penicillins or older cephalosporins against Staphylococcus spp. and Streptococcus spp., and it did not inhibit Streptococcus faecalis, Listeria, or anaerobic species. Ceftazidime was as active as ceftizoxime and moxalactam and more active than cefoperazone against Escherichia coli. Klebsiella, and Proteus mirabilis with minimal inhibitory concentrations of less than 0.2 mg/liter. Ceftazidime also inhibited Enterobacter, Citrobacter, Salmonella, and Shigella at concentrations below 0.2 mg/liter. Most Morganella, Proteus rettgeri, Proteus vulgaris, and Proteus inconstans were inhibited at concentrations below 1 mg/liter, similar to the concentrations for moxalactam, ceftizoxime, and cefotaxime. Ceftazidime was the most active agent tested against Pseudomonas aeruginosa, with a mean minimal inhibitory concentration of 1.6 mg/liter. It inhibited carbenicillin-, piperacillin-, cefoperazone-, and cefsulodin-resistant Pseudomonas. Minimal inhibitory and minimal bactericidal concentrations were similar, with the exception of some Pseudomonas values at 10(7) colony-forming units. Use of different media did not alter minimal inhibitory concentration values. Ceftazidime was not hydrolyzed by staphylococcal beta-lactamase or plasmid beta-lactamase of the TEM-1, TEM-2, SHV-1, OXA-1, PSE-1, PSE-2 types or by inducible beta-lactamases of the cephalosporinase type. Ceftazidime provides an extremely active agent against aerobic and facultative gram-negative bacteria.

Bacteria↗

Comparative in vitro activity of N-formimidoyl thienamycin against gram-positive and gram-negative aerobic and anaerobic species and its beta-lactamase stability.

The in vitro activity of N-formimidoyl thienamycin was determined against 800 gram-positive and gram-negative aerobic and anaerobic bacteria and compared with the activity of cefoxitin, cefazolin, cefamandole, cefotaxime, moxalactam, ampicillin, cefoperazone, and gentamicin. N-Formimidoyl thienamycin inhibited the majority of organisms at concentrations below 1 microgram/ml. It inhibited methicillin-resistant Staphylococcus aureus, Staphylococcus epidermidis, and Streptococcus faecalis. It inhibited beta-lactamase-producing Haemophilus influenzae and Neisseria gonorrhoeae. Unlike other new beta-lactams, it inhibited Listeria. Escherichia coli, Klebsiella pneumoniae, enterobacters, Serratia, indole-positive Proteus, Acinetobacter, Pseudomonas aeruginosa, and Bacteroides resistant to other agents were inhibited. There was minimal effect of inoculum size and aerobic versus anaerobic conditions, and serum had no effect on activity. Most minimal bactericidal concentrations were two- or fourfold greater than the minimal inhibitory concentration. N-Formimidoyl thienamycin showed partial synergy with aminoglycosides against S. aureus, S. faecalis, and many Pseudomonas and Enterobacteriaceae. It was not hydrolyzed by plasmid-mediated and chromosomal beta-lactamases.

Anaerobiosis↗

In vitro activity of apalcillin compared with that of other new penicillins and anti-Pseudomonas cephalosporins.

Apalcillin, a naphthydridine derivative of ampicillin, was compared with ticarcillin, azlocillin, mezlocillin, piperacillin, cefotaxime, and cefoperazone against gram-negative and gram-positive bacterial isolates and with cefsulodin and tobramycin against Pseudomonas aeruginosa. The minimal concentrations of apalcillin at which 50 and 90% of hospital isolates of Escherichia coli were inhibited were similar to those of mezlocillin and piperacillin (1.6 and 100 micrograms/ml, respectively). Apalcillin had minimal inhibitory concentrations similar to those of piperacillin against Citrobacter freundii and Citrobacter diversus. Against Klebsiella, apalcillin inhibited 50% of organisms at a concentration of 6.3 micrograms/ml, similar to piperacillin. The activity of apalcillin against Enterobacter (E. aerogenes, E. cloacae, and E. agglomerans) was similar to that of mezlocillin and piperacillin and greater than that of ticarcillin. The activity of apalcillin against Proteus mirabilis was similar to that of the other agents, as was its activity against indole-positive Proteus and Providencia. Only 40% of Serratia were inhibited at an apalcillin concentration of 25 micrograms/ml. Apalcillin was as active as piperacillin but twofold less active than cefoxitin or moxalactam against Bacteroides fragilis. It was as active as piperacillin, cefoperazone, and cefsulodin against P. aeruginosa (apalcillin inhibited 90% of organisms at a concentration of 25 mg/ml). There was an inoculum effect and a difference in the minimal inhibitory concentration and minimal bactericidal concentration with beta-lactamase strains. Apalcillin was hydrolyzed by plasmid beta-lactamase but not as well by cephalosporinases.

Ampicillin↗

In vitro activity of norfloxacin, a quinolinecarboxylic acid, compared with that of beta-lactams, aminoglycosides, and trimethoprim.

Norfloxacin is a quinolinecarboxylic acid compound. We examined the in vitro activity of this compound against gram-positive and -negative species, including anaerobic species. It inhibited 90% (MIC90) of strains of Escherichia coli at 0.05 microgram/ml, Klebsiella sp. at 0.4 microgram/ml, Salmonella and Shigella spp. at 0.1 microgram/ml, Citrobacter sp. at 0.4 microgram/ml, Enterobacter cloacae at 0.2 microgram/ml, Enterobacter aerogenes at 0.4 microgram/ml, and Enterobacter agglomerans at 0.2 microgram/ml. The MICs of Proteus mirabilis, Morganella sp., Proteus vulgaris, Proteus rettgeri, and Providencia sp. were 0.1, 0.2, 0.8, 0.3, and 1.6 micrograms/ml, respectively. The MIC90 of Serratia sp. was 1.6 micrograms/ml, and that of Acinetobacter sp. was 6.3 micrograms/ml. For Pseudomonas aeruginosa the MIC50, the MIC75, and the MIC90 were 0.8, 1.6, and 3.1 micrograms/ml, respectively. The MIC50 of Pseudomonas maltophilia was 3.1 micrograms/ml, and the MIC90 was 12.5 micrograms/ml. Yersinia, Arizona, and Aeromonas all were inhibited at concentrations below 1 microgram/ml, as was Campylobacter. The activity of the compound against gram-positive species was less impressive: the MIC90s of Staphylococcus aureus, Streptococcus pyogenes, Streptococcus agalactiae, and Streptococcus faecalis were 1.6, 6.3, 3.1, and 12.5 micrograms/ml, respectively. All Listeria strains were inhibited by 3.1 micrograms/ml. The activity of norfloxacine was not affected by the type of medium, pH, or inoculum size. There was no major difference between MIC and minimum bactericidal concentration values. Norfloxacin inhibited bacteria in every species which was resistant to ampicillin, carbenicillin, cephalexin, gentamicin, and trimethoprim at concentrations lower than those of aminothiazolyl cephalosporins, moxalactam, and aminoglycosides.

Aminoglycosides↗

In vitro activity and beta-lactamase stability of cefmenoxime.

The activity of cefmenoxime, an aminothiazolyl cephalosporin, was studied against 650 bacteria. It was slightly less active than cefotaxime and more active than moxalactam against staphylococci. It had activity similar to that of cefotaxime and ceftizoxime against group A and B streptococci and Streptococcus pneumoniae. It did not inhibit Streptococcus faecalis or Listeria spp. Cefmenoxime had activity similar to that of cefotaxime, ceftizoxime, ceftazidime, and moxalactam against Escherichia coli, Citrobacter diversus, Klebsiella, Proteus mirabilis, Salmonella, and Shigella. It inhibited beta-lactamase-positive and -negative isolates at less than or equal to 0.4 microgram/ml. Cefmenoxime was somewhat less active than moxalactam or ceftizoxime against Enterobacter cloacae, Enterobacter aerogenes, and Enterobacter agglomerans, but was more active than cefotaxime, ceftizoxime, or ceftazidime against Morganella (minimum inhibitory concentration for 90% of isolates, 0.1 microgram/ml.), Proteus vulgaris and Providencia spp. It was as active as ceftizoxime was against Serratia. Pseudomonas spp. and Bacteroides spp. were relatively resistant (minimum inhibitory concentration for 90% of isolates, greater than 100 micrograms/ml). The compound was stable to the common plasmid beta-lactamases, such as that of TEM. It was stable to most chromosomally mediated beta-lactamases, which act primarily as cephalosporinases, but was hydrolyzed by Bacteroides and Acinetobacter.

Aminoglycosides↗

Antibacterial activity and beta-lactamase stability of temocillin.

Temocillin, a 6-alpha-methoxy penicillin, inhibited 90% of strains of Escherichia coli, Klebsiella pneumoniae, Citrobacter, Proteus, Providencia, Salmonella, and Shigella at a concentration of less than or equal to 16 micrograms/ml. Haemophilus influenzae and Neisseria gonorrhoea were inhibited by less than or equal to 1 microgram/ml. Changing the medium or pH of the cultures did not alter the minimal inhibitory concentrations, which were similar in broth and human serum, as were the minimal bactericidal concentrations. An increase in inoculum size from 10(5) to 10(7) colony-forming units increased concentration required for inhibition. Temocillin inhibited strains resistant to ampicillin, ticarcillin, cefazolin, cefamandole, and cefoxitin. Most Pseudomonas aeruginosa strains and other Pseudomonas spp. and Acinetobacter spp. were resistant, as were gram-positive organisms. Temocillin was not hydrolyzed by the common plasmid and chromosomal beta-lactamases but inhibited them. The resistance of certain gram-negative bacilli to temocillin seemed to be a result of failure of the molecule to enter through the cell wall, since combination of temocillin with EDTA made Pseudomonas, Acinetobacter, and Enterobacter strains susceptible to low concentrations of the compound.

Bacteria↗