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PubMed1988

Influence of antibiotic therapy on faecal carriage of P-fimbriated Escherichia coli and other gram-negative bacteria in neonates.

The influence of previous antibiotic therapy on the aerobic faecal flora, including P-fimbriated Escherichia coli, was studied in 953 neonates at discharge from 22 neonatal wards in Sweden. Antibiotics, mainly ampicillin (with or without gentamicin) or cefuroxime, had been received by 37% of the infants. Treatment with ampicillin (with or without gentamicin) increased Klebsiella/Enterobacter and reduced Esch. coli colonization. Cephalosporin therapy (71% cefuroxime) reduced the frequency of colonization with both Esch. coli and Klebsiella/Enterobacter spp. but doubled the isolation rate of other Gram-negative bacteria (Citrobacter, Pseudomonas, Proteus and Acinetobacter spp.) and tripled the incidence of specimens yielding no aerobic Gram-negative growth. Gentamicin showed no significant ecological impact. The selection of Klebsiella/Enterobacter and P-negative Esch. coli strains by ampicillin was correlated with their resistance to this agent, while the association between P-fimbriated Esch. coli and cefuroxime therapy was not related to cefuroxime resistance.

Anti-Bacterial Agents↗

PubMed1989

Interactions of FCE 22101 with class I beta-lactamases.

Hyperproduction of chromosomal Class I beta-lactamase causes resistance to newer cephalosporins in Enterobacter cloacae, Citrobacter freundii, Serratia spp. and indole-positive Proteeae. We examined the interactions of FCE 22101 with these enzymes, measuring (i) antibiotic lability to pure enzyme, (ii) inducing power and (iii) activity against beta-lactamase-inducible strains and their -depressed and -basal mutants. Turnover numbers of FCE 22101 were between 0.7 and 1.5 molecules hydrolysed/min/enzyme molecule, compared with ranges of 0.5-40 for cefotaxime (950 for the Proteus vulgaris cephalosporinase) and 4400-22,000 for cephaloridine. FCE 22101 induced enzyme synthesis strongly below the MIC and antagonized labile weak inducers such as cefotaxime and mezlocillin. Like imipenem, but unlike newer cephalosporins, FCE 22101 had equal activity against inducible strains and derepressed mutants, and did not significantly select derepressed mutants from inducible populations. beta-Lactamase basal mutants of E. cloacae and C. freundii were four- to eight-fold more sensitive than inducible and derepressed organisms whereas beta-lactamase-basal, -inducible and -derepressed Proteeae and Serratia spp. were equally sensitive. This difference reflected the larger amounts of enzyme produced by the E. cloacae and C. freundii strains, rather than kinetic differences in enzyme activity.

Anti-Bacterial Agents↗

PubMed1989

In-vitro activity of FCE 22101 and synergy studies with other antimicrobial agents.

FCE 22101 is a penem antibiotic with broad in-vitro activity similar to that of imipenem, although less active against Pseudomonas aeruginosa. Combinations of FCE 22101 with ciprofloxacin or gentamicin against methicillin-resistant Staphylococcus aureus and methicillin-resistant Staph. epidermidis resulted in addition or indifference by the chequerboard method. The combination of FCE 22101 and gentamicin against Streptococcus faecalis was usually additive. Against Enterobacter cloacae FCE 22101 had MICs of 16 mg/l whilst in combination with gentamicin (0.25-0.12 mg/l) the MICs were reduced to less than 2 mg/l. Ciprofloxacin and FCE 22101 showed only addition against Enterobacter spp. similar results were obtained with the combinations of FCE 22101 and gentamicin or ciprofloxacin tested against Citrobacter freundii. With Serratia spp. FCE 22101 and gentamicin showed synergy, but FCE 22101 and ciprofloxacin showed indifference. Similar results were obtained with strains of Escherichia coli and Klebsiella, Proteus, and Providencia spp. FCE 22101 plus gentamicin, or aztreonam, against Ps. aeruginosa usually showed indifference, but with ciprofloxacin addition was the rule. In general the combination of FCE 22101 with other agents resulted in an additive rather than a synergistic effect.

Anti-Bacterial Agents↗

PubMed1989

Review of the in-vitro spectrum and characteristics of cefmetazole (CS-1170).

The in-vitro antimicrobial qualities of cefmetazole are summarized from a review of over 30 publications. Cefmetazole, a 7 alpha-methoxy cephalosporin, is shown to have an antimicrobial spectrum closely resembling cefoxitin's. However, cefmetazole is approximately two- to eight-fold more active than cefoxitin against commonly isolated species such as Escherichia coli, Klebsiella spp., Proteus mirabilis, Staphylococcus aureus, pyogenic streptococci, pneumococci, and Haemophilus influenzae. Cefmetazole is also active against anaerobic pathogens, Neisseria spp., Citrobacter diversus, indole-positive Proteus spp. and Branhamella catarrhalis. Cefmetazole is bactericidal against aerobic and anaerobic pathogens. Its MICs and MBCs are minimally influenced by high inoculum concentrations. beta-Lactamases failed to hydrolyze cefmetazole significantly and cefmetazole is considered the most stable of the cephamycin drugs. Some Bacteroides strains produce beta-lactamases that are uniquely inhibited by cefmetazole. In-vitro tests with cefmetazole have been evaluated and interpretive criteria established for NCCLS methods: susceptible greater than or equal to 18 mm (less than or equal to 8.0 mg/l) and resistant less than or equal to 14 mm (greater than or equal to 32 mg/l). The consistent cross-resistance and -susceptibility observed between cefmetazole and cefoxitin requires the testing of only one of these agents routinely. Quality control guidelines for cefmetazole disc diffusion (30 micrograms disc) and dilution tests are summarized in this review.

Bacteria↗

PubMed1989

In-vitro activity of FCE 22101 and other beta-lactam antibiotics against Enterobacteriaceae resistant to third generation cephalosporins.

The in-vitro activity of FCE 22101 was compared with those of imipenem, aztreonam, cefotaxime, ceftriaxone and latamoxef against 225 Enterobacteriaceae (209 clinical isolates and 16 derivatives of Escherichia coli K12) chosen for their resistance (MIC greater than or equal to 8 mg/l) to third-generation cephalosporins. The beta-lactamases produced by the strains of Enterobacter cloacae, Klebsiella pneumoniae and Esch. coli were identified. The mean MICs of FCE 22101 were 2-8 mg/l for Ent. cloacae, Citrobacter freundii and Morganella morganii. For Ent. cloacae, the MICs were slightly higher for the cephalosporinase non overproducing (5.5-8 mg/l) than for the cephalosporinase overproducing (4.5 mg/l) strains. The mean MIC was 9 mg/l for Serratia spp. but for half of the strains the MICs were greater than or equal to 16 mg/l. The MICs of FCE 22101 were 0.5-1 mg/l for the resistant clinical isolates or isogenic derivatives of K. pneumoniae and Esch. coli producing extended broad-spectrum beta-lactamases (SHV-2, SHV-3 or CTX-1), whether measured in the presence of clavulanate or not, and against the sensitive controls. This showed that the compound was not affected by these new beta-lactamases. The MICs of imipenem, on the average four to five times lower than those of FCE 22101, were found to be very similar for resistant and sensitive strains. The MICs of aztreonam were high (32-128 mg/l) for C. freundii, K. oxytoca and cephalosporinase overproducing strains of Ent. cloacae. There was cross-resistance between the third-generation cephalosporins, but the MICs of latamoxef remained low (1 mg/l) against M. morganii, Klebsiella spp. and Esch. coli.

Carbapenems↗

PubMed1989

Interactions of meropenem with class I chromosomal beta-lactamases.

Most newer penicillins and cephalosporins are labile to the Class I beta-lactamases that are inducible in Pseudomonas aeruginosa. Enterobacter spp., Citrobacter spp., Serratia spp. and indole-positive Proteeae, but fail to induce enzyme synthesis below the MIC. They remain active against the inducible strains but not against mutants (termed 'stably depressed') that manufacture beta-lactamase copiously without induction. Such mutants are segregated at high frequency and may be selected during therapy, sometimes causing clinical failure. Meropenem induced Class I enzymes weakly below the MIC in Ps. aeruginosa, Ent. cloacae, C. freundii, Ser. marcescens, Morganella morganii and Pr. vulgaris. Nonetheless it remained equally active against inducible strains and their derepressed mutants, and was no more active against laboratory-derived beta-lactamase basal mutants. It did not select derepressed mutants from beta-lactamase-inducible populations. These data suggested great stability to Class I beta-lactamases, and this deduction was confirmed by direct assays with purified beta-lactamases. Initial hydrolysis rates ranged from 0.9-10.0 drug molecules hydrolysed/enzyme molecule/minute but these values declined by 80-90% before 5% of the antibiotic had been hydrolysed, indicating that the carbapenem could deactivate the enzymes. Deactivation was reversible, full activity being restored once the meropenem was removed. These results suggest that meropenem, like imipenem and various experimental penems, may overcome the resistance problems presented by Class I beta-lactamases.

Bacteria↗

PubMed1989

Bactericidal activity of meropenem and interactions with other antibiotics.

MICs of meropenem for selected clinical isolates of bacteria were determined. Killing curves were performed on strains of methicillin-sensitive Staphylococcus aureus, methicillin-resistant Staph. aureus (MRSA), methicillin-resistant Staph, epidermidis, Escherichia coli, Klebsiella spp., Enterobacter cloacae, Pseudomonas aeruginosa, Citrobacter freundii and Acinetobacter spp. A reduction of greater than or equal to 3 x log10 in viable cells was observed at 4 and 6 h of exposure to 4 and 8 x MIC, and this was usually maintained at 24 h (with a few exceptions for methicillin-resistant Staph, epidermidis and Ent. cloacae). At the MIC and twice the MIC regrowth tended to occur at 24 h although this varied from strain to strain. The interaction with other antibiotics was determined by the chequerboard technique. Usually an additive or synergistic effect was observed when meropenem or imipenem was used in combination with an aminoglycoside against Gram-negative species, while in a few cases antagonism occurred in combination with beta-lactams. Against Staph, aureus, MRSA and Staph, epidermidis synergism was usually obtained with combinations with teicoplanin or vancomycin and either synergism or addition with combinations with rifampicin, co-trimoxazole or ciprofloxacin.

Anti-Bacterial Agents↗

PubMed1989

In-vitro activity of meropenem against clinical isolates in a multicentre study in Italy.

A multicentre in-vitro study was undertaken to evaluate the susceptibility of bacterial pathogens isolated in different Italian hospitals to meropenem. A total of 1399 aerobic and 452 anaerobic strains was analysed. Comparative agents were imipenem, cefotaxime, ceftazidime, ceftriaxone, piperacillin, ciprofloxacin, gentamicin, amikacin, plus vancomycin when appropriate. The MIC ranges (mg/l) of meropenem were: 0.015-2 for Klebsiella spp., Proteus spp., Morganella morganii and Providencia spp.; less than 0.008-1 for Escherichia coli; 0.016-32 for Serratia spp.; 0.03-2 for Enterobacter spp. and Citrobacter spp.; 0.03- greater than 128 for Acinetobacter anitratus; 0.03-32 for Pseudomonas spp.; less than 0.008-0.5 for Haemophilus spp. and Neisseria spp.; 0.015-64 for Staphylococcus spp.; 0.06- greater than 128 for Enterococcus spp.; less than 0.008-0.25 for Streptococcus spp.; 0.016-8 for Fusobacterium spp.; 0.03-8 for Bacteroides spp.; less than 0.06-0.5 for anaerobic Gram-positive cocci; 0.08-2 for Clostridium spp. Meropenem exhibited superior antibacterial activity against the aerobic and anaerobic strains tested when compared to the other beta-lactam drugs. The new carbapenem was as active as ciprofloxacin and more active than imipenem and the aminoglycosides against Enterobacteriaceae and Ps. aeruginosa. It was also more active than ciprofloxacin against most strains of Gram-positive cocci. Meropenem was slightly less potent than imipenem against staphylococci and enterococci, with the exception of oxacillin-susceptible Staph. aureus against which meropenem and imipenem exhibited similar antibacterial activity.

Aminoglycosides↗

PubMed1989

Ticarcillin/clavulanate in the treatment of severe peritonitis.

A prospective study was performed on 50 consecutive patients with secondary peritonitis. All patients received ticarcillin/clavulanate 5.2 g three times daily as initial antibiotic therapy. In 30 patients a primary perforation was found in the gastro-intestinal tract and 20 had post-operative peritonitis. In two thirds of the patients a diffuse peritonitis was found which affected the whole abdomen. Thirty-six patients underwent one or two laparotomies and 11 patients had more than three laparotomies. Subsequently, 17 patients died. The cause of death was a therapeutic failure as a result of the surgical procedure in ten patients (nine patients with persisting intestinal fistulae, one patient with bleeding), whereas in seven cases antibiotic therapy failed. Micro-organisms found in the latter patients were producers of type 1 beta-lactamase (Pseudomonas aeruginosa, Enterobacter sp., Citrobacter sp., Serratia marcescens) and enterococci. Ticarcillin/clavulanate is characterized by its broad antimicrobial spectrum against anaerobic and aerobic bacteria and seems, therefore, to be well suited for initial chemotherapy in patients with diffuse peritonitis.

Adult↗

PubMed1989

Clavulanate and beta-lactamase induction.

Concern has been expressed that clavulanate can antagonize ticarcillin against enterobacteria and pseudomonads that have inducible expression of chromosomal 'Class I' beta-lactamases. It is suggested that clavulanate-induced enzyme inactivates ticarcillin, which itself is a feeble inducer. We confirmed that this mechanism applied, showing that antagonism was abolished in beta-lactamase-basal mutants of inducible strains. Antagonism has been reported in double disc tests with strains of Pseudomonas aeruginosa, Enterobacter cloacae, Citrobacter freundii, Serratia spp. and indole-positive Proteeae. Only with some strains of Ent. cloacae and Morganella morganii, however, did the presence of 1-32 mg/l clavulanate elevate the MIC of ticarcillin by more than one or two dilutions in chequerboard studies. Clavulanate was synergistic with ticarcillin against Proteus vulgaris strains, being a potent inhibitor of the unusual Class I enzyme of this species. Induction-determined antagonism was not reduced in Ent. cloacae transconjugants that produced the plasmid-mediated TEM-1 beta-lactamase, despite the ability of this enzyme to bind clavulanate. Our results suggest that Ent. cloacae and M. morganii strains should be confirmed not to be more sensitive to ticarcillin alone than to ticarcillin/clavulanate, before the latter combination is used clinically. Otherwise, it appears that beta-lactamase induction is unlikely to cause significant antagonism. It is emphasized that induction is reversible, causing, at worst, a transient resistance. It should not be confused with the selection of stably-derepressed mutants that can occur, for example, in the clinical use of newer cephalosporins.

Bacteria↗

PubMed1990

Interactions of tazobactam and clavulanate with inducibly- and constitutively-expressed Class I beta-lactamases.

Clavulanate and tazobactam (YTR 830) were tested as inhibitors and inducers of the AmpC-type Class I beta-lactamases of Pseudomonas aeruginosa, Enterobacter cloacae, Citrobacter freundii, Serratia marcescens, Morganella morganii and the Ic beta-lactamase of Proteus vulgaris. Both clavulanate and tazobactam inhibited the Pr. vulgaris Class Ic beta-lactamase and potentiated ticarcillin and piperacillin against beta-lactamase derepressed variants of this species. Tazobactam, but not clavulanate, also had some ability to inhibit the AmpC Class I enzymes of M. morganii, C. freundii, Ps. aeruginosa, E. cloacae and S. marcescens. The piperacillin + tazobactam combination, unlike ticarcillin + clavulanate, showed some degree of synergy against most derepressed strains of these species. This behaviour partly depended upon the greater inhibitory activity of tazobactam for the enzymes, but also on piperacillin being easier to potentiate than ticarcillin. The synergy between piperacillin and tazobactam was greatest for M. morganii and C. freundii, least for Ps. aeruginosa and E. cloacae. Unfortunately, it is in the last two species that these enzymes pose the greatest resistance threat. Tazobactam caused little or no antagonism of piperacillin against beta-lactamase inducible species, whereas clavulanate antagonized ticarcillin against beta-lactamase inducible strains of E. cloacae and M. morganii (not other species). The antagonism of ticarcillin was attributable to beta-lactamase induction. The lack of antagonism with the tazobactam+piperacillin combination was related to tazobactam being a weaker inducer than clavulanate, not to piperacillin being less susceptible to antagonism than ticarcillin.

Bacteria↗

PubMed1990

The in-vitro activity of ceftibuten against 475 clinical isolates of gram-negative bacilli, compared with cefuroxime and cefadroxil.

The in-vitro activity of ceftibuten was compared with cefuroxime and cefadroxil against 475 clinically-significant, epidemiologically-distinct isolates of Gram-negative bacilli: 170 from blood, 212 from urine and 93 from a supplementary collection of multiply-resistant strains known to have resistance plasmids, to have caused sporadic or epidemic nosocomial infection, or both. Ceftibuten MICs ranged from 0.003 to greater than 32 mg/l, with a modal MIC of 0.01 mg/l: 95% of all isolates had ceftibuten MIC values of less than or equal to 8 mg/l, the sensitivity breakpoint suggested by the manufacturer. Ninety per cent of isolates had MICs of less than or equal to 1 mg/l and 49% had MICs of less than or equal to 0.03 mg/l. All isolates of Klebsiella, Serratia, Proteus and Providencia spp., and Morganella morganii had MIC values of 8 mg/l or less. Only two of 124 isolates of Escherichia coli tested, and only one of 23 Citrobacter spp., had MICs of greater than 8 mg/l (16, 16 and greater than 32 mg/l respectively). Resistance MIC greater than 16 mg/l) was more frequent among Enterobacter and Acinetobacter spp. Thirteen of 52 Enterobacter spp., and seven of 18 Acinetobacter calcoaceticus had MICs of at least 32 mg/l. MIC ranges, modal MICs and MIC90s indicated that ceftibuten was, with the exception of only two strains, consistently more active in-vitro than cefuroxime, which was in turn more active than cefadroxil.

Bacterial Infections↗

PubMed1990

In-vitro antibacterial activity of DQ-2556 and its stability to various beta-lactamases.

DQ-2556, a new cephalosporin, showed a broad antibacterial spectrum over Gram-positive and -negative organisms. The activity of DQ-2556 against recent clinical isolates of Gram-positive cocci and Enterobacteriaceae was comparable with that of cefpirome, and superior to that of ceftazidime. DQ-2556 was almost as active as cefpirome against Pseudomonas aeruginosa, but was less active than ceftazidime. With the exception of Ps. aeruginosa, DQ-2556 was bactericidal against various organisms at either the MIC or twice the MIC. DQ-2556 bound preferentially to penicillin-binding proteins (PBPs) 2, 1 and 3 of Staphylococcus aureus, PBPs 3, 1A and 1B of Escherichia coli and PBPs 1A, 3 and 4 of Ps. aeruginosa. DQ-2556 was stable to various penicillinases and cephalosporinases, but was unstable to oxyiminocephalosporinases. The Km values of DQ-2556 for the cephalosporinases of Citrobacter freundii and Enterobacter cloacae were only two- or three-fold higher than those of ceftazidime, indicating that DQ-2556 had a relatively high affinity for these enzymes compared with other recently developed cephalosporins. The MIC of DQ-2556 for Esch. coli increased four-fold in an OmpF-deficient mutant, indicating that the OmpF porin was one of the major routes for penetration of DQ-2556 into Esch. coli cells.

Ceftazidime↗

PubMed1990

A comparison of the mechanisms of decreased susceptibility of aztreonam-resistant and ceftazidime-resistant Enterobacteriaceae.

Twenty five strains of Enterobacteriaceae (five each of Enterobacter cloacae, Citrobacter freundii, Serratia marcescens, Morganella morganii and Providencia stuartii) were exposed to aztreonam and ceftazidime at 1/2 and 1 x MIC in liquid medium for 22 h, and also to 3, 5 and 10 x MIC and 16 mg/l of each agent in agar. Any putative mutant with an increase in the MIC of greater than or equal to 4 fold was examined for beta-lactamase expression and outer membrane protein profile. Mutants were selected on agar at approximately 10(7); however in liquid medium not all strains yielded mutants. Mutants lacking an outer membrane protein (OMP) with a molecular weight of 40,000 (+/- 5000) were selected with both agents, as were mutants expressing constitutive Richmond and Sykes Class 1 beta-lactamase. For the Ent. cloacae mutants increased beta-lactamase gave rise to MICs above the breakpoint of both agents, whereas with the other species ceftazidime susceptibility was more affected. Strains that were OMP- rarely had MICs above the breakpoint, unless there was also increased beta-lactamase expression, as in species such as M. morganii. Hence the major mechanism of resistance in these strains would appear to be beta-lactamase mediated rather than due to altered expression of outer membrane proteins.

Aztreonam↗

PubMed1990

Pefloxacin efficacy in gram-negative bacillary meningitis.

Sixteen patients with acute meningitis caused by Gram-negative bacteria were treated with pefloxacin intravenously. The age range of the patient group was six months to 85 years with a mean age of 40 years; three patients were children. In all but two patients meningitis was a complication of neurosurgical operations and fourteen of the sixteen had received prior therapy which was not successful. The causative organisms were: Pseudomonas aeruginosa (5), Acinetobacter calcoaceticus (4), Klebsiella pneumoniae (3), Enterobacter cloacae (2), Citrobacter diversus (1) and Salmonella group C (1). Pefloxacin was administered intravenously 800 mg twice a day to the adult patients (mean dosage of 21( +/- 6.7) mg/kg body weight) for a mean period ( +/- S.D.) of 11( +/- 4) days. The mean cerebrospinal fluid concentration of pefloxacin was 8.8( +/- 5.0) mg/l which was 54% of the mean peak serum concentration (16.3( +/- 8.8]. The mean MIC and MBC of the causative organisms were 1.1( +/- 1.2) mg/l and 1.64( +/- 1.2) mg/l. Thirteen patients (87%) were cured or clinically improved and twelve (80%) were bacteriologically cured. One patient failed, another patient had reinfection and one was not assessable. No side effects were observed. In the present study pefloxacin offered an efficacious and safe treatment of Gram-negative meningitis following failure of other antibiotic therapy.

Adolescent↗

PubMed1990

The in-vitro activity of cefodizime: a review.

For Enterobacteriaceae, MIC50s and MIC90s of cefodizime (mg/l), respectively, were as follows, for naturally non-beta-lactamase-producing species: Escherichia coli 0.12 and 0.5, Salmonella spp. and Shigella spp. 0.25 and 0.5, Proteus mirabilis 0.016 and 0.03; for chromosomal penicillinase-producing species. Klebsiella spp. 0.25 and 64, and for chromosomal cephalosporinase-producing species. Enterobacter cloacae 1 and 64, Citrobacter freundii 1 and 128, Serratia marcescens 2 and 8: indole-positive Proteus spp. 0.06 and 0.5; and Providencia stuartii 0.5 and 1. The activity of cefodizime was not modified by plasmid-mediated penicillinase-producing strains but cefodizime was inactive against cephalosporinase hyper-producing strains and against expanded broad-spectrum beta-lactamase-producing strains. Cefodizime was noticeably less active against Pseudomonas aeruginosa and Acinetobacter baumannii with MICs ranging from 32 to more than 128 mg/l. Haemophilus spp. and Neisseria gonorrhoeae, regardless of beta-lactamase producing status, as well as N. meningitidis, were highly susceptible (MIC50s and MIC90s less than or equal to 0.008 mg/l). Cefodizime was moderately active against methicillin-susceptible staphylococci (MIC50 and MIC90 8 mg/l) but failed to inhibit methicillin-resistant strains. Enterococci were generally resistant: Streptococcus pyogenes and Str. pneumoniae were inhibited by low concentrations (MIC50 and MIC90 0.12 and 0.5 mg/l). A fairly wide range of MICs was found for anaerobes, with lower values for Clostridium perfringens (MIC50 and MIC90 0.5 and 1 mg/l) than for Bacteroides fragilis (8- greater than 128 mg/l). These results show that cefodizime has similar properties to other third generation cephalosporins and suggest that cefodizime would find a role in the management of hospital infections.

Bacteria↗

PubMed1990

In-vitro activity of cefpodoxime against 1834 isolates from domiciliary infections at 20 UK centres.

A total of 1834 non-copy, general practice or outpatient isolates were collected by 20 hospital laboratories within the British Isles, and identified and tested for susceptibility to nine antimicrobial agents available by oral administration at one centre. Against Enterobacteriaceae cefpodoxime was the most active beta-lactam agent tested, the MIC90s being: for Escherichia coli 1.0 mg/l, for Proteus mirabilis 1.0 mg/l, for Citrobacter spp. 2.0 mg/l, and for Enterobacter spp., Serratia spp., Morganella spp. and Klebsiella spp. 16-64 mg/l. Cefpodoxime also showed a certain amount of activity against staphylococci and high activity against streptococci, the MIC90s being for Staphylococcus aureus 2 mg/l, for coagulase negative staphylococci 8 mg/l, for Streptococcus pyogenes 0.015 mg/l, for Str. pneumoniae 0.06 mg/l and for Str. agalactiae 0.5 mg/l.

Ceftizoxime↗

PubMed1991

In-vitro evaluation of ampicillin/brobactam and comparison with other beta-lactam antibiotics.

The ability of brobactam to inhibit beta-lactamases and the in vitro activity of ampicillin combined with brobactam was compared with another beta-lactamase inhibitor, clavulanic acid, and other beta-lactam antibiotics. Both inhibitors showed good and similar activity against staphylococcal penicillinase and most broad-spectrum beta-lactamases found in the Enterobacteriaceae, whether plasmid or chromosomally mediated. Both inhibitors were less active against chromosomally mediated cephalosporinases in Enterobacteriaceae, but brobactam was 8-50 times more potent than clavulanic acid. The amount and type of beta-lactamase produced by a particular bacterial strain was reflected in its sensitivity to a combination of ampicillin and brobactam, and correlated well with the sensitivity of extracted beta-lactamase to inhibition by brobactam. The in-vitro activity of ampicillin/brobactam in a 3:1 ratio was compared to amoxycillin/clavulanic acid (4:1 ratio), amoxycillin, cefaclor and cefuroxime. The two inhibitor combinations were generally of similar activity, but the brobactam combination had superior activity against Proteus vulgaris, Morganella morganii, Citrobacter freundii and Yersinia enterocolitica. The cephalosporins were less effective against the Bacteroides fragilis group, Prot. vulgaris and M. morganii, but had advantages in the case of Escherichia coli, Klebsiella spp. and C. diversus. The MBC of ampicillin/brobactam was similar to the MIC. No resistant sub-populations were observed amongst the staphylococcal strains investigated. Exposure of bacteria to sub-inhibitory levels of ampicillin/brobactam did not lead generally to the development of resistance.

Ampicillin↗