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1.  Plasmid-coded ampicillin resistance in Haemophilus ducreyi. 
Seven of the 96 ampicillin-resistant isolates of Haemophilus ducreyi reported in the preceding article (Bilgeri et al., Antimicrob. Agents Chemother. 22:686-688, 1982) were investigated and found to harbor plasmids of 3.95, 5.2, 5.8, and 6.4 megadaltons. All except the 5.8-megadalton plasmid have been shown to code for beta-lactamase. The 6.4- and 5.2-megadalton plasmids of three isolates were conjugally transferable to a streptomycin-resistant mutant of H. ducreyi at high frequencies, perhaps due to the presence in these strains of a high-molecular-weight plasmid.
PMCID: PMC183815  PMID: 6983859
2.  S-Adenosyl-L-methionine: macrocin O-methyltransferase activities in a series of Streptomyces fradiae mutants that produce different levels of the macrolide antibiotic tylosin. 
A series of mutants of Streptomyces fradiae selected for increased production of the macrolide antibiotic tylosin was analyzed for levels of expression of macrocin O-methyltransferase, the enzyme which catalyzes the final step in the biosynthesis of tylosin. Increased tylosin production was accompanied by increased macrocin O-methyltransferase in some of the mutants. Increased expression of macrocin O-methyltransferase was due to more rapid early biosynthesis of the enzyme, to reduced decay of enzyme specific activity late in the fermentation, or to combinations of both. Mutant strains which showed rapid loss of enzyme specific activity late in the fermentation converted large amounts of tylosin to relomycin. The most productive mutants, which synthesized elevated levels of macrocin O-methyltransferase, also produced large amounts of macrocin, the substrate for the enzyme. Incomplete conversion of macrocin to tylosin by these mutants may be due to substrate and product inhibition (E. T. Seno and R. H. Baltz, Antimicrob. Agents Chemother. 20:370-377, 1981). The results suggest that both the levels of precursors and the levels of expression of tylosin biosynthetic enzymes are important for efficient production of tylosin.
PMCID: PMC182007  PMID: 7103455
3.  Structural and phenotypic varieties of gentamicin resistance plasmids in hospital strains of Staphylococcus aureus and coagulase-negative staphylococci. 
We previously described a neonatal nursery epidemic of infections caused by a single strain of Staphylococcus aureus bearing a gentamicin resistance plasmid (Vogel et al., Antimicrob. Agents Chemother. 13:466-472, 1978). The same plasmid was present in two isolates of Staphylococcus epidermidis from the patients in this nursery and was transferable interspecifically from either S. aureus or S. epidermidis. During the ensuing 3 years, in the absence of further epidemics, we collected 162 gentamicin-resistant strains of S. aureus and coagulase-negative staphylococci from patients distributed throughout our hospital. Gentamicin resistance plasmids obtained from 41 representative S. aureus and coagulase-negative staphylococcal strains differed as determined by phenotypic and molecular analyses from the plasmid in the neonatal nursery epidemic. Nevertheless, these plasmids were structurally related to each other and to the plasmid of the original epidemic. Our results suggest an evolutionary relationship among these plasmids and support the hypothesis of a genetic reservoir of gentamicin resistance in coagulase-negative staphylococci transferable to S. aureus.
PMCID: PMC182010  PMID: 7103456
4.  Comparison of cefoperazone with penicillin, ampicillin, gentamicin, and chloramphenicol in the therapy of experimental meningitis. 
Cefoperazone was compared with penicillin against Streptococcus pneumoniae, gentamicin against Escherichia coli, and ampicillin and chloramphenicol against Haemophilus influenzae in the therapy of experimental meningitis in rabbits. Meningitis was produced by intracisternal inoculation into cerebrospinal fluid, and all antibiotics were administered intravenously over 8 h in dosages that would achieve serum levels comparable to those found in humans. The mean percent penetration into purulent cerebrospinal fluid, expressed as (cerebrospinal fluid concentration/serum concentration) x 100%, was 2.6% for penicillin, 22.0% for gentamicin, 12.1% for ampicillin, 23.8% for chloramphenicol, and 6.4% for cefoperazone. The mean cerebrospinal fluid antibiotic concentrations exceeded the minimum bactericidal concentration for the test strain in each experimental model, except for ampicillin in experimental meningitis due to the beta-lactamase-producing H. influenzae. Cefoperazone produced a significantly faster bactericidal effect after 4 h of treatment when compared with penicillin (P = 0.037) and ampicillin (P = 0.01) in meningitis caused by S. pneumoniae and H. influenzae (ampicillin susceptible), respectively. In meningitis caused by E. coli, cefoperazone was significantly (P = 0.006) more rapidly bactericidal after 8 h of treatment when compared to gentamicin. In addition, cefoperazone was significantly more rapidly bactericidal than either ampicillin or chloramphenicol in experimental meningitis due to beta-lactamase-producing H. influenzae. Cefoperazone deserves further evaluation in the therapy of bacterial meningitis in humans.
PMCID: PMC183809  PMID: 6217785
5.  Comparative In Vitro Activities of N-Formimidoyl Thienamycin and Moxalactam Against Nonfermentative Aerobic Gram-Negative Rods 
N-Formimidoyl thienamycin was the most active drug against strains of Pseudomonas aeruginosa with a 90% minimum inhibitory concentration of 1.25 μg/ml. With the exception of P. maltophilia, thienamycin was as active or more active than moxalactam against other species of pseudomonads and against other genera of nonfermenters.
PMCID: PMC181966  PMID: 6211143
6.  In vitro susceptibility of cephalothin-resistant Enterobacteriaceae and Pseudomonas aeruginosa to Amikacin and selected new beta-lactam agents. 
Amikacin was evaluated in vitro by agar dilution testing against 148 different clinical isolates of cephalothin-resistant Enterobacteriaceae and Pseudomonas aeruginosa in parallel with cephalothin, cefoxitin, moxalactam, N-formimidoyl thienamycin, ceftriaxone, and cefmenoxime. Cefsulodin was also evaluated against 39 isolates of P. aeruginosa. More than 80% of all isolates tested were also gentamicin resistant, as determined by disk testing. Moxalactam and amikacin had comparable high activities against Proteus species, Escherichia coli, Serratia species, and Providencia species, and both amikacin and N-formimidoyl thienamycin had comparably high activities against the Klebsiella-Enterobacter group. N-Formimidoyl thienamycin was the most active agent against P. aeruginosa, followed by cefsulodin and amikacin.
PMCID: PMC182006  PMID: 6213196
7.  Effects of azlocillin in combination with clavulanic acid, sulbactam, and N-formimidoyl thienamycin against beta-lactamase-producing, carbenicillin-resistant Pseudomonas aeruginosa. 
We investigated the effects of the combination of azlocillin with the beta-lactamase inhibitors clavulanic acid and sulbactam and with N-formimidoyl thienamycin against strains of Pseudomonas aeruginosa with R-factor-mediated carbenicillin resistance. The 10 strains tested (1 R-, 9 R+) were isogenic, except for the presence of individual plasmids determining each of nine plasmid-mediated beta-lactamases found in P. aeruginosa. We utilized a checkerboard technique for testing antibiotic combinations. Low concentrations of clavulanic acid produced synergy with azlocillin against the strains producing the TEM-1, TEM-2, PSE-1, PSE-3, and PSE-4 beta-lactamases; for the strains producing the OXA-1, OXA-2, OXA-3, and PSE-2 beta-lactamases, such synergy was not found. With sulbactam, synergy was demonstrated in all strains except that producing PSE-2 beta-lactamase; for several strains, however, the concentration of sulbactam required to produce synergy was substantially higher than that for clavulanic acid. N-Formimidoyl thienamycin was highly active as a single agent against all of the strains, regardless of beta-lactamase production. The combination of N-formimidoyl thienamycin and azlocillin produced synergy against only two of the strains tested.
PMCID: PMC183723  PMID: 6100423
8.  Randomized comparative study of moxalactam and cefazolin in the treatment of acute urinary tract infections in adults. 
Eighty-nine patients with clinical and laboratory evidence of acute urinary tract infection were randomized to therapy with either moxalactam (500 mg) or cefazolin (1 g) every 12 h. Escherichia coli was the predominant pathogen in both groups (92.6 versus 90.2%). Therapy was continued for 3 days after the patient defervesced. The minimum hospital stay was 5 days. Sequential urine cultures were obtained on day 3, at discharge, and 5 to 10 days after the cessation of therapy. THe average duration of hospital stay was 5.6 days for both groups of patients. THe incidence of recurrent infection was similar in uncomplicated patients (9.1 versus 10%) and in complicated patients with a condition predisposing them to urinary tract infections (43 versus 42%). Moxalactam-treated patients had a higher incidence of reversible hepatic enzyme elevation (36%) and Streptococcus faecalis superinfections (12.2%). Moxalactam is as effective as cefazolin for the elimination of gram-negative pathogens from the urine of patients with acute urinary tract infections, but it is associated with a higher incidence of reversible side effects.
PMCID: PMC183669  PMID: 6214996
9.  Treatment of experimental herpes simplex virus encephalitis with (E)-5-(2-bromovinyl)-2'-deoxyuridine in mice. 
(E)-5-(2-Bromovinyl)-2'-deoxyuridine (BVDU) was examined for its ability to increase the survival rate of mice infected intracerebrally with herpes simplex virus type 1 (strain KOS). BVDU was administered orally (through the drinking water), intraperitoneally, or subcutaneously at doses ranging from 40 to 400 mg/kg per day, starting 0, 2, 4, or 6 days postinfection. Regardless of the route of administration, BVDU effected a significant reduction in the mortality rate of mice infected with herpes simplex virus type 1 if treatment was initiated shortly after virus infection, i.e., day 0 or 2 (or day 4, if BVDU was administered subcutaneously) postinfection, at a dosage of 80 mg/kg per day or higher. Similar beneficial effects were noted with orally administered BVDU in mice inoculated intraperitoneally or intranasally with herpes simplex virus type 1. These findings establish the therapeutic efficacy of BVDU in the systemic treatment of herpes simplex virus type 1 encephalitis in mice.
PMCID: PMC183760  PMID: 7137983
10.  Trapping of nonhydrolyzable cephalosporins by cephalosporinases in Enterobacter cloacae and Pseudomonas aeruginosa as a possible resistance mechanism. 
Resistance to cefotaxime (CTA) and ceftriaxone (CTR) in Enterobacter cloacae and Pseudomonas aeruginosa was investigated in several strains which are susceptible or resistant to these agents. All strains produced a chromosomally mediated cephalosporinase of the Richmond type 1. beta-Lactamases in susceptible strains were inducible, whereas resistant strains produced the enzymes constitutively. CTA and CTR were very poor substrates but potent inhibitors of all enzymes. Binding to, rather than hydrolysis by, beta-lactamases was assumed to be a major reason for resistance, and combination experiments supported this assumption. Dicloxacillin, which did not inhibit the growth and which was a poor inducer but a strong inhibitor of these beta-lactamases, exerted strong synergistic activity when combined with CTA or CTR in strains which produced large amounts of beta-lactamase constitutively. Cefoxitin, on the other hand, poorly active alone, but a good inducer, strongly antagonized CTA or CTR in susceptible strains producing inducible enzymes. In marked contrast to CTA and CTR were the findings with cefsulodin. Cefsulodin was active against CTA- and CTR-resistant Pseudomonas, and its activity was hardly influenced by dicloxacillin or cefoxitin. Since cefsulodin was found to have a very low affinity for all cephalosporinases, these findings corroborate the assumption that binding of nonhydrolyzable cephalosporins, rather than hydrolysis by cephalosporinases, may play an important role in resistance to these agents and other newer cephalosporins in Enterobacteriaceae, as well as in other gram-negative bacteria.
PMCID: PMC181998  PMID: 6808912
11.  Clinical efficacy of cefotaxime in serious infections. 
Thirty-five patients underwent 38 treatment courses with cefotaxime. Documented infections included 11 bacteremias, 7 cases of nosocomial pneumonia, 6 surgical wound infections, 3 bone infections, 1 biliary infection, and 1 urinary tract infection. Granulocytopenic patients with fever received 15 courses of empiric cefotaxime therapy alone; in 8 courses, no definite site of infection or pathogen was isolated. Broad-spectrum antibiotics had been administered to 23 patients before cefotaxime. Thirty-seven bacterial pathogens were isolated from 25 patients. Three such pathogens were resistant to cefotaxime and required alternative therapies. Pathogenic isolates included 13 Serratia marcescens, 12 Pseudomonas aeruginosa, 4 Escherichia coli, 2 Klebsiella pneumoniae, 2 Providencia stuartii, 1 Enterobacter cloacae, 1 Haemophilus influenzae, 1 Enterococcus, and 1 Staphylococcus aureus. Of the treatment courses, 25 of 38 resulted in a favorable response to cefotaxime, including 9 of 15 in granulocytopenic patients. Superinfection was seen in one patient. The emergence of resistance was documented in another patient. Of 15 patients with multiply resistant pathogens, 12 improved with cefotaxime. Of 12 patients with Pseudomonas aeruginosa, 6 favorably responded. Possible complications of cefotaxime were observed in 14 of 42 treatment courses. Cefotaxime is most useful in treatment of infections due to multiply resistant, gram-negative pathogens other than Pseudomonas aeruginosa.
PMCID: PMC181838  PMID: 6282202
12.  Comparative in vitro activity of ceftriaxone against anaerobic bacteria. 
The in vitro activity of ceftriaxone was compared with those of other recently introduced beta-lactam antimicrobial agents (cefoperazone, cefotaxime, and moxalactam) and with those of cefoxitin, clindamycin, and metronidazole against 227 strains of anaerobic bacteria. The data obtained in this investigation suggest that ceftriaxone, like a majority of the new beta-lactam antimicrobial agents, may be of limited value in the treatment of serious infections involving anaerobic bacteria.
PMCID: PMC183738  PMID: 6100430
13.  Activities of various beta-lactams and aminoglycosides, alone and in combination, against isolates of Pseudomonas aeruginosa from patients with cystic fibrosis. 
The inhibitory and bactericidal activities of carbenicillin, ticarcillin, moxalactam, cefoperazone, azlocillin, piperacillin, ceftazidime, and three aminoglycosides, alone and in various combinations, were determined against 60 isolates of Pseudomonas aeruginosa from the sputum of patients with cystic fibrosis. Ceftazidime was the most active beta-lactam, with minimum inhibitory and bactericidal concentrations for 90% of isolates of 4 micrograms/ml. Moxalactam was the least active of the new beta-lactams, with activity equivalent to that of carbenicillin; each had a minimum inhibitory concentration for 90% of isolates of 64 micrograms/ml and a minimum bactericidal concentration for 90% of isolates of 128 microgram/ml. All combinations of an aminoglycoside plus a beta-lactam showed favorable inhibitory effects. Combinations of beta-lactams showed mostly addition or indifference. Although little antagonism was seen with combinations of beta-lactams or with aminoglycoside-beta-lactam combinations, no consistent advantage of beta-lactam combinations was demonstrated in vitro. These results suggest several single drugs and combinations that merit clinical evaluation in cystic fibrosis patients with Pseudomonas pulmonary infections.
PMCID: PMC182049  PMID: 6810757
14.  Mutational Enzymatic Resistance of Enterobacter Species to Beta-Lactam Antibiotics 
Mutants with enhanced β-lactam resistance were selected from strains of Enterobacter cloacae and E. aerogenes by using three antibiotics. High-level β-lactamase-producing mutants had similar degrees of increased resistance, enzyme substrate profiles, and isoelectric (pI) values irrespective of the selective agent. Reverse mutants from a resistant E. cloacae mutant regained the susceptibility pattern originally exhibited by the wild type, or were of enhanced susceptibility, and no longer expressed increased β-lactamase production. β-Lactamases of the mutants were similar in pI values to the wild-type enzyme. The increased resistance of the mutants therefore appeared to be accounted for by increased β-lactamase production.
PMCID: PMC181960  PMID: 6979311
15.  Comparative in vitro study of temocillin (BRL 17421), a new penicillin. 
The activity of temocillin (BRL 17421), a new penicillin, was tested in vitro against 653 isolates of gram-negative bacilli and gram-positive cocci. The drug was compared with other beta-lactam antibiotics and tobramycin. It inhibited the majority of gram-negative bacilli tested except for Pseudomonas aeruginosa and Acinetobacter calcoaceticus, which were highly resistant. It was active against more than 50% of the multiresistant strains tested. Temocillin was more active than mezlocillin against most gram-negative bacilli and more active than moxalactam, ceftriaxone, and ceftazidime against Enterobacter spp. In general, it was slightly less active than the other drugs tested and had no activity against the gram-positive cocci. There was no significant change in drug activity when pH and medium were varied, and the effect of serum binding was minimal. There was no significant inoculum effect when the size of the inoculum was increased from 10(4) to 10(6) organisms per ml.
PMCID: PMC181957  PMID: 6919412
16.  Emergence of resistance to beta-lactam and aminoglycoside antibiotics during moxalactam therapy of Pseudomonas aeruginosa infections. 
In four patients with Pseudomonas aeruginosa infections, the infecting strain developed resistance to moxalactam during therapy with this drug. In addition, P. aeruginosa isolates from two of these four patients showed increased resistance to aminoglycosides. Isolates from a third patient acquired cross-resistance to other antipseudomonal beta-lactams. In three of the cases, disk susceptibility tests failed to detect the resistance that was demonstrated in broth dilution assays. Isolate identities were confirmed by serotyping. No new plasmids were found by agarose gel electrophoresis. The mechanisms for this resistance did not involve enzymatic antibiotic degradation. These findings suggest that currently available expanded-spectrum cephalosporin derivatives should probably not be used alone for most serious infections due to P. aeruginosa. They also suggest that strains with multiple antibiotic resistance may become more prevalent in hospitals if these drugs are used extensively.
PMCID: PMC185717  PMID: 6218778
17.  Antimicrobial activity of amikacin combinations against Enterobacteriaceae moderately susceptible to third-generation cephalosporins. 
Enterobacteriaceae strains having elevated minimal inhibitory concentrations (greater than or equal to 2.0 to less than or equal to 32 micrograms/ml) of cefoperazone, cefotaxime, ceftazidime, and moxalactam were synergistically inhibited by amikacin combinations (54.1 to 69.6% occurrence). Indifference was rare (8.1% for moxalactam), and true antagonistic interactions were not observed. Strains resistant or susceptible to these new cephalosporins were also synergistically inhibited by the addition of amikacin, reducing resistant cephalosporin minimal inhibitory concentrations to clinically achievable levels.
PMCID: PMC185706  PMID: 7159071
18.  Comparative pharmacokinetics of ceftazidime and moxalactam. 
The pharmacokinetics of ceftazidime and moxalactam were compared after intravenous and intramuscular administration of single 1-g doses to eight healthy volunteers in a crossover study. The bioavailability of the antibiotics after administration by either route was almost complete. Both drugs had similar areas under the serum curves. Significant differences between ceftazidime and moxalactam were observed with respect to the apparent volume of distribution (18.4 and 24.1 liters, respectively), to the terminal half-life (1.6 versus 2.0 h), and to urinary recovery of the active compound (96 versus 79%). Ceftazidime was almost completely eliminated by renal excretion (greater than 96%), whereas about 20% of the moxalactam was eliminated by nonrenal mechanisms. The concentrations of ceftazidime and moxalactam in serum after a 1-g dose exceeded the concentrations required to inhibit 90% of the Enterobacteriaceae for about 8 and 10 h, respectively. The levels of ceftazidime and moxalactam in serum exceeded the 90% minimal inhibitory concentration of Pseudomonas aeruginosa for about 6 and 1 h, respectively.
PMCID: PMC183718  PMID: 6765416
19.  Moxalactam pharmacokinetics in children. 
We measured the serum concentrations of moxalactam in 10 children receiving antibiotic prophylaxis for surgery and in 18 children treated for documented or suspected infections. Moxalactam was administered intravenously at a dose of 50 mg/kg every 8 h. After the first dose in 28 patients, mean moxalactam concentrations 5 min, 30 min, 2 h, and 8 h after infusion were 257, 177, 82.2, and 17.5 micrograms/ml, respectively. The mean half-life (T 1/2) was 2.44 h (range: 0.55 to 7.96 h). The mean distribution volume (VD) was 0.30 liters per kg. No significant accumulation was observed with multiple doses. Prophylactic and therapeutic groups had similar serum levels, T 1/2, and VD. The five infants less than 1 year of age had a lower mean 30-min level (P less than 0.01), larger VD (P less than 0.001) and longer T 1/2 (P less than 0.025) than the children older than 1 year. A dose of 50 mg/kg produced 30-min levels in excess of 64 microgram/ml in all patients studied, but 8-h trough levels were below the minimal inhibitory concentrations breakpoint of 17 mg/ml in 32% of patients.
PMCID: PMC183672  PMID: 6214997
20.  In vitro comparison of N-formimidoyl thienamycin (MK0787) and Azlocillin with three aminoglycosides and ticarcillin against Pseudomonas aeruginosa. 
The activities of N-formimidoyl thienamycin and azlocillin were compared with those of tobramycin, gentamicin, amikacin, and ticarcillin against 175 Pseudomonas aeruginosa isolates, including 24 strains with known mechanisms of resistance to aminoglycosides. The 50% mean inhibitory concentration for azlocillin was lower than for ticarcillin, but the 90% mean inhibitory concentration was similar for both drugs. All susceptible and multidrug-resistant strains were susceptible to N-formimidoyl thienamycin.
PMCID: PMC181971  PMID: 6805426
21.  Cefaclor pharmacokinetic parameters: serum concentrations determined by a new high-performance liquid chromatographic technique. 
Pharmacokinetic parameters of cefaclor were studied in eight patients after an oral dose of 250 mg. Serum samples were obtained before and on 19 occasions after oral administration. Cefaclor serum concentrations were determined by a new high-performance liquid chromatographic technique.
PMCID: PMC181848  PMID: 7081972
22.  In vitro activity of new beta-lactam antibiotics and other antimicrobial drugs against anaerobic isolates from obstetric and gynecological infections. 
The in vitro activities of N-formimidoyl thienamycin, clindamycin, chloramphenicol, metronidazole, cefoperazone, cefotaxime, cefoxitin, moxalactam, penicillin G, and piperacillin were determined against 158 anaerobic bacteria isolated from endometrial wash cultures of women with pelvic infections. In general, N-formimidoyl thienamycin was the most active, with all organisms inhibited by less than or equal to 0.5 microgram/ml. Chloramphenicol, clindamycin, and metronidazole inhibited all organisms by less than or equal to 8 microgram/ml. The penicillins and cephalosporins exhibited variable activity of lesser degrees.
PMCID: PMC183823  PMID: 7181484
23.  Comparative efficacies of ceftriaxone, moxalactam, and ampicillin in experimental Salmonella typhimurium infection. 
The activities of ceftriaxone, moxalactam, and ampicillin against Salmonella typhimurium LT-2 were compared in culture media at pH 5, 6, 7 and 8 and in mice inoculated intraperitoneally. The minimal inhibitory concentrations for strain LT-2 in Mueller-Hinton broth were 0.03 microgram of ceftriaxone per ml, 0.08 microgram of moxalactam per ml, and 0.4 microgram of ampicillin per ml. A comparison of minimal inhibitory concentrations in buffered broth at pH 5 with those in media at higher pH values showed that ceftriaxone was more acid stable than the other antibiotics. Groups of CF-1 female mice inoculated intraperitoneally with 3 X 10(4) colony-forming units received saline or each drug in fourfold decremental doses by the subcutaneous route every 8 h for 3 days, beginning at 24 h after challenge. The mean log 10 colony-forming units of S. typhimurium per spleen at the end of treatment and the mortality rates at 21 days after inoculation were measured for each treatment group. The mean log 10 colony-forming units per spleen was significantly reduced from that of the saline control by dosages of greater than or equal to 0.06 mg of ceftriaxone per kg, 64 mg of moxalactam per kg, or greater than or equal to 16 mg of ampicillin per kg (P less than 0.05). Mortality rates of infected mice were significantly reduced by dosages of greater than or equal to 1 mg of ceftriaxone per kg or greater than or equal to 64 mg of ampicillin per kg (P less than 0.05), whereas moxalactam in dosages as high as 16 mg/kg did not significantly reduce mortality rate. These results demonstrate the superiority of ceftriaxone to the other tested antibiotics on a weight basis in this model of experimental Salmonella infection.
PMCID: PMC183731  PMID: 6100426
24.  Efficacy of a twelve-hourly ceftriaxone regimen in the treatment of serious bacterial infections. 
Eighteen patients with 21 serious infections were treated with ceftriaxone, 1 g intravenously every 12 h, for a mean duration of 8 days. Eighteen gram-negative and two gram-positive organisms were isolated. Sites of infection included blood (three patients), urinary tract (six patients), respiratory tract (seven patients), biliary tract (three patients), ascitic fluid (one patient), and skin (one patient). Serum, bile, and ascitic fluid concentrations of ceftriaxone were in excess of the minimal bactericidal concentration required for the infecting organism in all cases. A bacteriological response was demonstrated in 94% of the infections. A clinical response occurred in four infections from which no pathogens were recovered. In one patient, ceftriaxone failed to eradicate a peritoneal infection due to Bacteroides fragilis. In two patients, superinfection with enterococci developed both during and after therapy. Systemic tolerance to ceftriaxone was excellent.
PMCID: PMC183681  PMID: 6289735
25.  Comparative in vitro activities of beta-lactam-tobramycin combinations against Pseudomonas aeruginosa and multidrug-resistant gram-negative enteric bacilli. 
Piperacillin was more consistently active than tobramycin, carbenicillin, moxalactam, or ceftriaxone against strains of Pseudomonas aeruginosa isolated from blood cultures and against multidrug-resistant strains. Moxalactam and ceftriaxone were more consistently active than tobramycin, carbenicillin, or piperacillin against multidrug-resistant Enterobacteriaceae. Synergy between beta-lactam antibiotics and tobramycin was frequently observed against strains of P. aeruginosa isolated from blood cultures but not against multidrug-resistant organisms. Piperacillin plus tobramycin was the most active antibiotic combination against P. aeruginosa. Moxalactam plus tobramycin and ceftriaxone plus tobramycin were the most active antibiotic combinations against Enterobacteriaceae.
PMCID: PMC182062  PMID: 6810755

Results 1-25 (444)