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PubMed1993

Identification of a novel plasmid-mediated beta-lactamase with chromosomal cephalosporinase characteristics from Klebsiella pneumoniae.

A clinical isolate of Klebsiella pneumoniae resistant to a wide variety of beta-lactams, including third generation cephalosporins, aztreonam and cephamycins, as well as to beta-lactam/clavulanate and sulbactam combinations was examined. It was found that this resistance was transmissible to Escherichia coli recipients via a small 5.3 MDa plasmid encoding for an unusual beta-lactamase produced in relatively large quantities. The enzyme, designated LAT-1, exhibited a highly basic isoelectric point (pI = 9.4) and its hydrolytic activity resembled closely that of a class-I chromosomal cephalosporinase. In vitro, LAT-1 hydrolysed cephaloridine, cephalothin and cephalexin more rapidly than penicillins. A slow hydrolysis of cefoxitin, ceftibuten, ceftazidime and cefotaxime was also observed. The enzyme was inhibited by low concentrations of aztreonam and cloxacillin but it was virtually unaffected by clavulanate. Under stringent conditions, the LAT-1 encoding plasmid did not hybridize with probes specific for TEM-1 and Enterobacter cloacae AmpC beta-lactamase genes. The plasmid was not self-transferable but was readily mobilized by a conjugative R-plasmid harboured by the same K. pneumoniae strain.

Anti-Bacterial Agents↗
PubMed1993

Extended-spectrum beta-lactamases in Escherichia coli and Klebsiella spp. in European septicaemia isolates.

Five per cent of Escherichia coli and klebsiella septicaemia isolates from the European Study Group on Antibiotic Resistance (ESGAR) study in 1987 to 1988 showed reduced susceptibility or resistance to cefotaxime, ceftazidime and/oraztreonam. Six of 15 isolates studied were susceptible to cefoxitin and MICs of cefuroxime, cefotaxime, ceftazidime and aztreonam were reduced by clavulanic acid. The isoelectric points of their beta-lactamases were in the range of 5.3-7.6. DNA hybridization showed that four of these beta-lactamases belonged to the TEM or SHV family. Transfer of cefotaxime resistance by conjugation was seen in two of the strains. Nine strains were resistant to cefoxitin (MIC > 16 mg/L) and MICs of cefuroxime, cefotaxime, ceftazidime and aztreonam were only slightly reduced in the presence of clavulanic acid. All nine strains produced at least one beta-lactamase of chromosomal origin with pI > 8.4, and four of these strains also harboured beta-lactamases with a pI range of 6.6-8.2. Cefoxitin resistance could be transferred by conjugation in one strain. Thus E. coli and Klebsiella spp. from the ESGAR septicaemia isolates were found to produce extended-spectrum beta-lactamases of both chromosomal and plasmid origin.

Anti-Bacterial Agents↗
PubMed1995

Potent activity of meropenem against Escherichia coli arising from its simultaneous binding to penicillin-binding proteins 2 and 3.

A mutant strain of Escherichia coli with reduced susceptibility to imipenem, designated TL2740, was selected following serial passage of the parent strain, E. coli C600, in broth containing increasing concentrations of the carbapenem; the MIC of imipenem for TL2740 was eight-fold greater than that of the parent strain. The mutant also exhibited reduced susceptibilities to panipenem and biapenem and high-level resistance to mecillinam, but was as susceptible to meropenem, ceftazidime, piperacillin and the other beta-lactams tested as strain C600. The affinity of penicillin-binding protein (PBP) 2 of TL2740 for imipenem and meropenem was ten-fold less than that of C600, thereby providing an explanation for the mutant's reduced susceptibility to some carbapenems and mecillinam. However, this theory was confounded by the observation that the in-vitro activities of meropenem against both parent and mutant strains were virtually the same and by the fact that PBP 2 is the principal target of the antibiotic. Imipenem and aztreonam, which bind to PBP 2 and PBP 3 respectively, demonstrated synergic activity when tested in combination against both C600 and TL2740. These results suggest that the potent activity of meropenem against the mutant strain might also be due to a synergic effect resulting from simultaneous binding to both PBP 2 and PBP 3 and that the variable activities of the carbapenems against TL2740 were related to their different PBP binding profiles. Compared with C600, TL2740 appeared shorter on electron microscopy and had a longer generation time, discrepancies which are compatible with defective PBP 2 activities in the mutant strain. We also identified three clinical isolates of E. coli with beta-lactam susceptibility profiles which resembled that of TL2740 i.e. high-level resistance to mecillinam and low-level resistance to carbapenems, with the exception of meropenem to which these strains were susceptible; in common with TL2740, the combination of imipenem and aztreonam was synergic against these isolates. The genetic basis of resistance in all of the mecillinam-resistant strains, including TL2740, mapped close to lip at 15' on the E. coli chromosome with transductional analysis. The results strongly suggest that the reduced susceptibilities of the clinical isolates to carbapenems were due to mutations in the genes encoding the PBP 2s of these strains which affected their affinities for beta-lactam antibiotics.

Bacterial Outer Membrane Proteins↗
PubMed1995

Extended-spectrum plasmid-mediated beta-lactamases.

Extended-spectrum beta-lactamases (ESBLs) are mutant enzymes which derive from TEM or SHV (class A) enzymes. They confer variable levels of resistance to cefotaxime, ceftazidime and other broad-spectrum cephalosporins and to monobactams such as aztreonam but have no detectable activity against cephamycins and carbapenems. Recently, new plasmid-mediated ESBLs, not derived from TEM or SHV enzymes but related to cephalosporinases of Enterobacteriaceae (class C enzymes), that confer resistance to all cephalosporins including cephamycins, have been reported. However, to date there have been no reported outbreaks due to strains producing transferable cephalosporinases. Klebsiella pneumoniae is the species in which the ESBL enzymes have been most commonly reported around the world. Most of the clinical isolates that produce TEM- or SHV-derived ESBL, come from hospitalised patients and have frequently caused nosocomial outbreaks. Care should be taken in the selection of a beta-lactam for the treatment of infections because the presence of an ESBL does not prevent other mechanisms of resistance, such as decreased permeability, from emerging. Broad-spectrum cephalosporins including cefepime and cefpirome are hydrolysed by ESBL. However, low level resistance to cefotaxime, ceftriaxone, cefepime and aztreonam does occur in some strains producing certain TEM-derived ESBL. It remains to be seen, therefore, whether such isolates are clinically susceptible to these drugs. The combination of a third-generation cephalosporin and a beta-lactamase inhibitor such as sulbactam could be of interest against some strains producing certain ESBLs. Among the 7-alpha-methoxy cephalosporins, cefotetan and latamoxef are the most active. However, cephamycins should be used with caution to treat infections caused by ESBL-producing K. pneumoniae because of the relative ease with which clinical strains decrease the expression of outer membrane proteins. The most active beta-lactams are the carbapenems, imipenem and meropenem, which are highly resistant to hydrolysis by TEM and SHV related beta-lactamases. Meropenem is intrinsically the more active agent, with MICs (0.03-0.12 mg/L) generally lower than those of imipenem (0.06-0.5 mg/L) and appears stable to all the beta-lactamases belonging to class A or C, including those with an extended-spectrum against third-generation cephalosporins.

Carbapenems↗
PubMed1996

Imipenem and cephem resistant Pseudomonas aeruginosa carrying plasmids coding for class B beta-lactamase.

From October 1988 to January 1992, nine isolates of Pseudomonas aeruginosa carrying transferable plasmids encoding imipenem-hydrolyzing beta-lactamase (pI = c. 9.5) were recovered from nine different patients in a neurosurgical ward of a hospital in Japan. The beta-lactamase activities of the sonicated extracts from the transconjugants were inhibited by EDTA and this was partially reversible by the addition of zinc cation. The substrate specificity and pI of the beta-lactamase were similar to those of the metallo beta-lactamases from P. aeruginosa and Serratia marcescens TN9106. All strains were resistant to imipenem, carbenicillin and antipseudomonal cephems including ceftazidime, cefsulodin, cefpirome, while four and five strains were susceptible to piperacillin and aztreonam, respectively. Both low level imipenem resistance and high level cephem resistance were co-transferred with the production of metallo beta-lactamase, while resistance to piperacillin, aztreonam, and high level imipenem-resistance were not selected. Production of chromosomal cephalosporinase in piperacillin resistant strains was derepressed, and production of outer membrane protein of D2 was diminished in highly imipenem resistant strains. Six strains were isolated in 1991, and the amounts of antipseudomonal agents, especially imipenem, used in the neurosurgical ward increased markedly in this year. Only three of the nine isolates had the same serotype, pyocin type and phage type. Our results suggest that the repeated isolation of imipenem and cephem-resistant P. aeruginosa producing metallo beta-lactamase was related to the high usage of antipseudomonal beta-lactam antibiotics such as imipenem, and was exacerbated by the dissemination of a plasmid.

Anti-Infective Agents↗
PubMed1997

The effect of antimicrobial agents on the induction of tumour necrosis factor by alveolar macrophages in vitro in response to endotoxin.

Alveolar macrophages from New Zealand white rabbits were incubated with twice the MIC of amikacin, ciprofloxacin, aztreonam, ceftazidime and imipenem and exposed to either 10(4), 10(5) or 10(6) cfu/mL live Pseudomonas aeruginosa ATCC 27853 or 0.1, 1 or 10 mg/L purified lipopolysaccharide (LPS) derived from P. aeruginosa to determine the effects of different classes of antimicrobial agent on production of tumour necrosis factor (TNF). Incubation of macrophages with ciprofloxacin and amikacin resulted in less TNF activity after exposure to live P. aeruginosa than was found for saline, aztreonam, ceftazidime or imipenem (P < 0.05). However, no significant differences were found between any of the agents after macrophages had been exposed to purified LPS. Different antimicrobial agents therefore appear to exert different effects in vitro on the TNF response of macrophages to bacterial stimulation.

Animals↗
PubMed1998

Comparison of a novel, inhibitor-potentiated disc-diffusion test with other methods for the detection of extended-spectrum beta-lactamases in Escherichia coli and Klebsiella pneumoniae.

A novel, inhibitor-potentiated disc-diffusion test for detecting extended-spectrum beta-lactamases (ESBLs) in bacteria was evaluated. This test uses the principle of augmentation (by > or = 10 mm) of inhibition zones produced by ceftazidime, cefotaxime, ceftriaxone or aztreonam discs on Mueller-Hinton agar supplemented with clavulanate (4 mg/L). The test was initially compared with the double-disc synergy test, Kirby-Bauer disc-diffusion test and Etest ESBL screen with a panel of 45 reference strains with known resistance profiles. This panel consisted of 27 ESBL-positive Escherichia coli strains expressing 14 Bush group 2be enzymes and 18 other E. coli and Klebsiella pneumoniae strains (14 non-ESBL beta-lactamase producers and four non-beta-lactamase producers). The Kirby-Bauer disc-diffusion test was the least sensitive method: 11-44% of the ESBL-positive control strains were misclassified as susceptible to ceftazidime, cefotaxime, ceftriaxone or aztreonam when interpreted by National Committee for Clinical Laboratory Standards (NCCLS) criteria. The sensitivities of the inhibitor-potentiated disc-diffusion test, the double-disc synergy test (when discs were 25 or 30 mm apart) and the Etest ESBL screen (with a breakpoint of > 4-fold reduction in ceftazidime MIC in the presence of clavulanate) were 100%, 96% and 89-96%, respectively. The inhibitor-potentiated disc-diffusion test was further evaluated with 81 E. coli and K. pneumoniae clinical isolates, which were identified as putative ESBL-producers by the double-disc synergy test. For these isolates, the sensitivity of both the inhibitor-potentiated disc-diffusion test and the Etest ESBL screen was 100%. In conclusion, the inhibitor-potentiated disc-diffusion test is a sensitive, convenient and inexpensive method of screening for ESBLs in E. coli and K. pneumoniae isolates, with potential for incorporation into routine clinical laboratory service.

Anti-Bacterial Agents↗
PubMed1999

In-vitro susceptibility of 1982 respiratory tract pathogens and 1921 urinary tract pathogens against 19 antimicrobial agents: a Canadian multicentre study. Canadian Antimicrobial Study Group.

A total of 3903 pathogens from 48 Canadian medical centres were tested against 19 antimicrobial agents. Five agents showed activity against > or = 90% of all 1982 respiratory tract pathogens tested (ciprofloxacin, 90%; cefoperazone, 91%; ticarcillin/clavulanate, 92%; ceftazidime and imipenem, 93% each). Nine agents had > or = 90% activity against Enterobacteriaceae from respiratory tract infection (cefotaxime and ticarcillin/clavulanate, 90% each; aztreonam, ceftizoxime and ceftriaxone, 91% each; ceftazidime, 93%; ciprofloxacin, 97%; imipenem and netilmicin, 98% each). Similarly, five agents had activity against > or = 90% of all 1921 urinary tract pathogens tested (ciprofloxacin and ticarcillin/clavulanate, 90% each; cefoperazone and netilmicin, 91% each; imipenem, 99%). Nine agents had > or = 95% activity against Enterobacteriaceae from urinary tract infection (ciprofloxacin, 95%; cefotetan, 97%; aztreonam, cefotaxime, ceftazidime, ceftizoxime, ceftriaxone and netilmicin, 98% each; imipenem, 99%). Seventeen agents had activity against > or = 95% of Staphylococcus aureus strains. Susceptibility of Pseudomonas aeruginosa isolates ranged from 2% to 91%.

Acinetobacter↗
PubMed2001

Natural antimicrobial susceptibilities of Plesiomonas shigelloides strains.

The natural susceptibility of 74 Plesiomonas shigelloides strains isolated from humans (n = 50), water (n = 22) and animals (n = 2) to 71 antibiotics was examined. MICs were performed using a microdilution procedure with Mueller-Hinton broth and an inoculum of 1 x 10(6) cfu/mL. Plesiomonas strains were naturally susceptible or naturally susceptible and intermediate to tetracyclines, several aminoglycosides, aminopenicillins in combination with beta-lactamase inhibitors, all cephalosporins except cefoperazone, ceftazidime and cefepime, carbapenems, aztreonam, quinolones, trimethoprim, sulfamethoxazole, azithromycin, chloramphenicol, nitrofurantoin and fosfomycin. Uniform natural resistance was found to all penicillins tested, roxithromycin, clarithromycin, lincosamides, streptogramins, glycopeptides and fusidic acid. Plesiomonas strains were naturally resistant and intermediate to streptomycin, erythromycin and rifampicin. There were two susceptibility patterns to piperacillin/tazobactam, several cephalosporins and aztreonam. In contrast to a previous study with beta-lactam antibiotics, susceptibility testing of non-beta-lactams revealed no alterations of the MICs of most antibiotics, using different inocula and media. A database is described of the natural susceptibility of P. shigelloides strains to a wide range of antibiotics. It can be used for the validation of susceptibility test results of these bacteria.

Animals↗
PubMed2005

Differential effects of beta-lactams on human IFN-gamma activity.

OBJECTIVES: To investigate whether a range of beta-lactam antibiotics conjugate to and hence reduce the activity of IFN-gamma, as has been shown for penicillin G. A selection of penicillins, cephalosporins, a monobactam (aztreonam), a beta-lactamase inhibitor (clavulanic acid), a carbapenem (meropenem) and the non-beta-lactam penicillin derivative d-penicillamine were tested for their effect on IFN-gamma activity. METHODS: Following exposure to a range of concentrations of these compounds, for varying lengths of time, IFN-gamma activity was assayed by induction of CD54 on the surface of the lung epithelial cell line A549, utilizing an ELISA. RESULTS: Clavulanic acid, cefoxitin and cefaloridine were the most potent inhibitors of IFN-gamma activity, followed by cefotaxime, ceftriaxone and phenoxymethylpenicillin. Ampicillin was less inhibitory than penicillin G, whilst meropenem and aztreonam had the least effect and d-penicillamine had no effect. The modulatory effect of these compounds was not due to a direct effect on CD54 induction. Unlike freshly prepared drugs, aged preparations of penicillin G and clavulanic acid had no significant effect on IFN-gamma activity. CONCLUSIONS: beta-Lactams differ in their capacity to modulate human IFN-gamma activity. This finding may have implications for the immunomodulatory effects of beta-lactams and for the design both of beta-lactams that do not affect the immune system and those which may be used therapeutically to target cytokine action.

Anti-Bacterial Agents↗
PubMed1992

Trimethoprim/sulfamethoxazole remains active against enterotoxigenic Escherichia coli and Shigella species in Guadalajara, Mexico.

Bacterial isolates obtained from fecal cultures of U.S. adults in Guadalajara, Mexico, with diarrhea developing during the summers of 1987, 1988, and 1989 were tested for in vitro antimicrobial susceptibility. No resistance was seen among 220 enterotoxigenic Escherichia coli isolates nor among 89 Shigella strains to aztreonam, norfloxacin, ciprofloxacin, gentamicin, or furazolidone. High level (greater than 1000 micrograms/ml) resistance to trimethoprim/sulfamethoxazole (TMP/SMX) was found in 7% of E. coli and 3% of Shigella strains. Susceptibility patterns of 27 E. coli strains derived from fecal cultures of Mexican infants in Guadalajara with diarrhea during the same time period showed similar results, possibly reflecting the presence of a common microbial reservoir. The study serves as a baseline for newer antimicrobials (fluoroquinolones and aztreonam) where no resistance is currently seen and provides evidence of the continuing value of TMP/SMX for therapy of diarrhea among travelers to Gudalajara and perhaps other areas of Mexico.

Diarrhea↗
PubMed1991

State of penicillin-binding proteins and requirements for their bactericidal interaction with beta-lactam antibiotics in Serratia marcescens highly resistant to extended-spectrum beta-lactams.

The quantities of penicillin-binding proteins (PBPs), and sensitivity to extended-spectrum beta-lactams, were measured in isogenic strains of Serratia marcescens with high (HR) and low (LR) resistance to extended-spectrum beta-lactam antibiotics and with constitutively overproduced chromosomal beta-lactamase in the periplasm. The binding of structurally different beta-lactams to PBPs in growing resistant bacteria was determined quantitatively. In S. marcescens HR, the amounts of PBPs 3 and 6 were, respectively, 1.5 and 2 times those in strain LR and in sensitive reference strains. Sensitivities of the essential PBPs in S. marcescens LR and HR to the tested beta-lactams were identical. Only a single target, PBP 3, was highly sensitive to cefotaxime, ceftazidime and aztreonam. In contrast, three PBPs (2, 1A and 3) were highly sensitive to imipenem. In growing S. marcescens HR and LR, all antibiotics, even at fractions of their minimal growth inhibitory concentrations (MICs), bound extensively to those PBPs which were highly sensitive to them. Thus, overproduced beta-lactamase did not prevent PBP-beta-lactam interaction. Only at or above their (high) MICs did cefotaxime, ceftazidime and aztreonam bind to multiple targets. Growth inhibition of the otherwise highly resistant S. marcescens HR at the lower MIC of imipenem was correlated with the binding of this antibiotic to multiple, highly sensitive targets in the bacteria. Killing of the bacteria by inactivation of multiple targets was suggested. This assumption was supported by the synergistic killing of HR bacteria by combinations of the PBP-2-specific mecillinam with PBP-3-specific beta-lactams.

Anti-Bacterial Agents↗
PubMed2005

Dissemination of transferable CTX-M-type extended-spectrum beta-lactamase-producing Escherichia coli in Korea.

AIMS: Among 365 Escherichia coli isolated in 2003, 31 cefotaxime-resistant isolates were obtained from clinical specimens taken from adults hospitalized in Busan, Korea. Six extended-spectrum beta-lactamase (ESBL)-producing isolates were investigated further to determine the mechanism of resistance. METHODS AND RESULTS: These isolates were analysed by antibiotic susceptibility testing, pI determination, plasmid profiles, transconjugation test, PCR-restriction fragment length polymorphism (RFLP), enterobacterial repetitive consensus (ERIC)-PCR and DNA sequencing. All six of these isolates were found to contain the CTX-M-type ESBL genes. Five clinical isolates and their transconjugants produced CTX-M-3. One clinical isolate (K17391) and its transconjugant (trcK17391) produced CTX-M-15. Five clinical isolates also produced another TEM-1. One clinical isolate (K12776) also contained another TEM-52. CTX-M-3 ESBL gene was responsible for the resistance to piperacillin, cephalothin, cefotaxime, cefepime and aztreonam. CTX-M-15 or TEM-52 was especially responsible for the resistance to ceftazidime. CONCLUSIONS: These results appear to represent the in vivo evolution of CTX-M-type beta-lactamase genes (bla(CTX-M-3) --> bla(CTX-M-15)) under the selective pressure of antimicrobial therapy (especially ceftazidime). PCR-RFLP is a reliable method to discriminate CTX-M-15 gene from CTX-M-3 gene. ERIC-PCR analysis revealed that dissemination of CTX-M-3 was not due to a clonal outbreak of a resistant strain but to the intra-species spread of resistance to piperacillin, cephalothin, cefotaxime, cefepime and aztreonam in Korea. SIGNIFICANCE AND IMPACT OF THE STUDY: This is the first report of the occurrence of CTX-M-1 cluster ESBLs in Korea. A more comprehensive survey of these ESBL types from Korea is urgently needed because of the in vivo evolution of CTX-M-15 from CTX-M-3. The emergence of these CTX-M-type ESBLs suggests that diagnostic laboratories should screen for ESBLs with ceftazidime as well as cefotaxime; they should still perform clavulanate synergy tests on resistant isolates.

Adult↗
PubMed1999

In vitro assessment of colistin's antipseudomonal antimicrobial interactions with other antibiotics.

OBJECTIVE: To study the interactions of colistin (MIC 2 mg/L) at concentrations of 0.5 and 5 mg/L with ceftazidime (1 and 75 mg/L, MIC 0.5 mg/L), aztreonam (1 and 30 mg/L, MIC 0.12 mg/L), meropenem (1 and 25 mg/L, MIC 0.03 mg/L), gentamicin (1 and 10 mg/L, MIC 2 mg/L), piperacillin (5 and 100 mg/L, MIC 4 mg/L) and ciprofloxacin (0.25 and 4 mg/L, MIC 1 mg/L) using a representative strain of Pseudomonas aeruginosa isolated from a cystic fibrosis patient. METHODS: The method used was a bacterial time kill curve with single agents and combinations. Using inocula of 106 CFU/mL, multiple sampling was performed over 6 h and in triplicate. The AUBKC of the time versus viable count curve, with single agents and combinations of agents, was taken as the endpoint for comparison. RESULTS: For colistin plus ceftazidime, colistin plus aztreonam, colistin plus meropenem and colistin plus ciprofloxacin, the pattern was for all the combinations (high or low concentrations) to produce smaller AUBKCs than single agents. In experiments using a bacteriostatic agent such as ceftazidime, the AUBKCs (log CFU/µL per h) for colistin 0.5 mg/L or 5 mg/L alone were 32.3±0.8 or 12.7±0.5, and for ceftazidime 1 mg/L or 75 mg/L alone they were 24.3±1.5 or 20.9±2.7. Combinations of colistin 0.5 mg/L plus either ceftazidime 1 mg/L or 75 mg/L produced AUBKCs of 23.8±1.8 or 16.1 mg/L. Combinations of colistin 5 mg/L plus ceftazidime 1 mg/L or 75 mg/L produced AUBKCs of 12.2±0.8 or 8.7±1.0. The AUBKCs for colistin 5 mg/L plus 75 mg/L are significantly smaller than those for the single agents, indicating synergy. In experiments using the bactericidal agent ciprofloxacin, the AUBKCs (log CFU/mL per h) for colistin 0.5 mg/L or 5 mg/L alone were 33.6±1.9 or 11.2±2.4, and for ciprofloxacin 0.25 mg/L or 4 mg/L alone they were 32.8±1.3 or 5.0±0.7. Combinations of colistin 0.5 mg/L plus either ciprofloxacin 0.25 mg/L or 4 mg/L produced AUBKCs of 32.2±0.9 or 4.3±1.4. Combinations of colistin 5 mg/L plus ciprofloxacin 0.25 mg/L or 4 mg/L produced AUBKCs of 10.7±1.5 or 4.2±0.6. Although combination AUBKCs were smaller than those for single agents, in no case did this reach statistical significance (p<0.05). CONCLUSIONS: These studies indicate that addition of colistin to other antipseudomonal drugs tends to produce smaller AUBKCs and hence greater killing of Pseudomonas aeruginosa than monotherapy.

Journal Article↗
PubMed1994

Outbreak of extended-spectrum beta-lactamase producing Serratia marcescens in an intensive care unit.

Serratia marcescens has recently been identified as an important etiological agent in nosocomial infections, and is considered to be an opportunistic pathogen agent in immunosuppressed patients undergoing long periods of intensive care. Research carried out in 1991 and 1992 showed that it was of epidemiological relevance in only 1-2% of clinical isolates at the Ospedale di Circolo, Varese, Italy. However, between 7 February and 11 October 1993, the incidence of cases attributable to S. marcescens had increased to 5%; 157 strains of Serratia marcescens were isolated from clinical specimens of 43 patients admitted to an intensive care unit; these strains, characterized by epidemic spread, showed the same pattern of multiresistance to antibiotics including monobactams and oxyimino-cephalosporins. During the same period 23 isolates were also recovered from 18 patients admitted to wards other than the intensive care unit; these strains, characterized by a wide range of antibiotic susceptibility, were also sensitive to beta-lactam antibiotics with the exception of first generation cephalosporins. The production of extended-spectrum beta-lactamases (ES beta Ls) and their genetic determinism were studied. All the epidemic strains of S. marcescens resistant to ceftazidime, cefotaxime, ceftriaxone and aztreonam produced three different beta-lactamases with pI 5.4, 5.5 and 8.4 respectively. In contrast, non-epidemic strains produced only a beta-lactamase with pI 8.4. The beta-lactamase with pI 5.5 was plasmid-mediated, hydrolizing ceftazidime and aztreonam, showing it to be an ES beta L; while the beta-lactamase with pI 5.4, although plasmid-mediated, did not hydrolize monobactams or oxyimino-cephalosporins.(ABSTRACT TRUNCATED AT 250 WORDS)

Cross Infection↗
PubMed1986

Antibiotic susceptibility of Haemophilus influenzae isolated from cerebrospinal fluid and blood.

The emergence of ampicillin and chloramphenicol resistant Haemophilus influenzae type b in Denmark has created demands for alternative treatments of serious infections with H. influenzae. In this study 102 strains of H. influenzae recovered from cerebrospinal fluid (85) and blood (17) were tested for susceptibility to ampicillin, piperacillin, erythromycin, rifampicin, chloramphenicol, cefuroxime, cefotaxime, ceftazidime, ceftriaxone, moxalactam, aztreonam, and netilmicin by means of the agar dilution method. The majority (97%) was H. influenzae type b and of these strains 94% belonged to biotype I. Nine of the investigated strains were beta-lactamase producers. Ceftriaxone and cefotaxime were the most active agents (MIC90 less than or equal to 0.025 microliter/ml) followed by moxalactam and aztreonam (MIC90 = 0.1 microgram/ml). Except for ampicillin and piperacillin, the MIC was similar for beta-lactamase producers and non-producers. Several of the investigated antibiotics, especially some of the third generation cephalosporins, might constitute valid therapeutical alternatives to conventional drugs in the treatment of severe H. influenzae infections.

Anti-Bacterial Agents↗
PubMed1989

[The study on Pseudomonas aeruginosa infection in a hospital--2. Bacteriological study].

We investigated the hospital acquired infection of P. aeruginosa in urological wards by determining the serotype and testing the sensitivity of this bacteria to antibiotics. The results were as follows: 1. 92 strains of G-serotype (22.2%), 76 of A-serotype (18.3%) and 65 of B-serotype (15.7%) were predominantly found in the serotype distribution of 415 P. aeruginosa strains isolated from urine or feces. 2. Comparing the sensitivity of P. aeruginosa to various antibiotics determined by MIC50 (the concentration to inhibit growth of 50% of the objective bacteria), Dibekacin showed MIC50 of 0.78 microgram/ml, Ceftazidime 1.56 micrograms/ml, Cefsulodin 3.13 micrograms/ml, and Polymixin-B, Piperacillin, Aztreonam 6.25 micrograms/ml. The analysis of the relationship between serotype and sensitivity to antibiotics demonstrated that K-serotype of P. aeruginosa tended to be highly sensitive and M-serotype be less sensitive to only Dibekacin. There was no definite relation of serotype to sensitivity against any other antibiotics. The comparison of sensitivity to antibiotics determined by MIC50,80 between P. aeruginosa isolated from urine and that from feces revealed that the former was less sensitive by one to four grades than the latter. The sensitivity of P. aeruginosa isolated from feces at admission was not different from that at discharge. In the chronological changes in sensitivity of P. aeruginosa isolated from urine, the strains highly resistant to Cefsulodin, Ceftazidime, Aztreonam and Dibekacin had increased in 1984 and 1985. 3. These highly resistant strains tended to break out in the urological wards, which suggested the need for more intensive prophylactic measures against hospital acquired infection.

Cross Infection↗
PubMed1983

In vitro antibacterial activity and beta-lactamase stability of E-0702, a new cephalosporin.

The in vitro activity of E-0702 was compared with the in vitro activity of cefotaxime, ceftazidime, moxalactam, and aztreonam against 600 gram-positive and gram-negative aerobic and anaerobic isolates. E-0702 had a minimal inhibitory concentration for 50% of isolates (MIC50) of 25 micrograms for Staphylococcus aureus, 50 micrograms for Staphylococcus epidermidis, and 1.6 to 3.1 micrograms for streptococci, with Streptococcus faecalis resistant. E-0702 had MIC50s against Escherichia coli, Klebsiella pneumoniae, and Enterobacter aerogenes comparable to those of cefotaxime, ceftazidime, moxalactam, and aztreonam, but MIC90S were higher than those of the other agents. It was as active as the other agents against Proteus mirabilis, Salmonella spp., and Shigella spp., but was four- to eightfold less active against Citrobacter freundii, Enterobacter cloacae, Providencia spp., Morganella spp., and Proteus vulgaris, with isolates in each species resistant. Activity against Bacteroides fragilis was fourfold less than that of cefoxitin. E-0702 was hydrolyzed by plasmid beta-lactamases and was only a weak inhibitor of plasmid and chromosomal beta-lactamases. There was an inoculum effect for E. cloacae, Serratia spp., Morganella spp., and Pseudomonas spp.

Bacteria↗