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PubMed1984

Comparative in vitro activities of enoxacin (CI-919, AT-2266) and eleven antipseudomonal agents against aminoglycoside-susceptible and -resistant Pseudomonas aeruginosa strains.

The in vitro activity of enoxacin (CI 919, AT 2266), a new oral quinolone carboxylic acid compound, was compared with those of gentamicin, tobramycin, amikacin, azlocillin, piperacillin, aztreonam, moxalactam, imipenem, cefsulodin, ceftazidime, and cefoperazone against 101 aminoglycoside-susceptible and 105 aminoglycoside-resistant Pseudomonas aeruginosa strains. Among these 206 P. aeruginosa isolates were 25 strains with known mechanisms of resistance to amikacin. The activity of enoxacin was similar to that of tobramycin against aminoglycoside-susceptible strains, with MICs of 1.0 to 2.0 micrograms/ml and 0.5 to 1.0 microgram/ml, respectively, for 90% of the strains. Enoxacin was the most active agent in this in vitro study against aminoglycoside-resistant P. aeruginosa strains, with MICs of 2.0 to 4.0 micrograms/ml for 90% of the strains. Strains with enzymatic resistance to amikacin were more resistant to beta-lactams (except enoxacin and imipenem) than were strains with decreased permeability.

Aminoglycosides↗
PubMed1985

In vitro susceptibilities of isolates from patients with Branhamella catarrhalis pneumonia compared with those of colonizing strains.

Branhamella catarrhalis has recently been recognized as an opportunistic respiratory pathogen. We tested 10 isolates recovered from patients with documented B. catarrhalis pneumonia and 15 colonizing isolates for their susceptibility to 19 antimicrobial agents and for their ability to produce beta-lactamase. Eight of ten disease isolates and 12 of 15 colonizing isolates produced a detectable beta-lactamase. The isolates that were negative for beta-lactamase were susceptible to all agents tested, including penicillin G. Although all strains were found to be susceptible to the majority of the newer agents by broth dilution testing, the most active new semisynthetic penicillin was azlocillin (MIC that inhibited 90% of strains, 0.5 micrograms/ml), and moxalactam had the greatest potency among the cephalosporins (MIC that inhibited 90% of strains, 0.06 micrograms/ml). Members of the first- and second-generation cephalosporins had only moderate activity. All disease isolates were susceptible to the aminoglycosides and to trimethoprim-sulfamethoxazole and resistant to vancomycin. The antibiotic susceptibilities of the disease isolates were not different from those of the colonizing strains. The results of standardized disk diffusion testing did not correlate well with those of dilution testing for penicillin or ampicillin. However, disk diffusion testing did predict susceptibility adequately for the remainder of the antibiotics tested.

Aminoglycosides↗
PubMed1985

In vitro antibacterial activities of antibiotics against Pseudomonas aeruginosa in peritoneal dialysis fluid.

Intraperitoneal antibiotics are used to treat Pseudomonas aeruginosa peritonitis, a serious complication of continuous ambulatory peritoneal dialysis. However, P. aeruginosa killing is often inefficient despite low MBCs. Broth dilution MIC/MBC and time kill curves of tobramycin, amikacin, netilmicin, azlocillin, piperacillin, ceftazidime, cefsulodin, and ciprofloxacin were determined in peritoneal dialysis fluid (PDF), buffered PDF, fluid recovered from patients on continuous ambulatory peritoneal dialysis (RPF), and cation-supplemented Mueller-Hinton broth. MBCs of all antibiotics were 8 to 16 times greater in PDF and RPF than in Mueller-Hinton broth or buffered PDF. Use of the time kill curve technique and Mueller-Hinton broth showed that aminoglycosides killed greater than or equal to 99.9% of P. aeruginosa at 1 h, ciprofloxacin killed greater than or equal to 99.9% at 2 h, and beta-lactams killed greater than or equal to 99.9% at 6 h. In contrast, killing was not demonstrated in PDF by any drug at 6 h and by aminoglycosides only at 24 h. Bactericidal activity was optimal in RPF for ciprofloxacin at 1 h and for aminoglycosides at 2 h; bactericidal activity was not demonstrated in RPF with any beta-lactam (no kill by penicillins; less than 99% kill by cephalosporins). Slow bacterial growth, increased protein binding, and glucose concentrations and other inhibitors may interfere with beta-lactam activity in RPF. These considerations and reported clinical failures and toxicity of aminoglycoside therapy warrant further study of quinolones and drug combinations in P. aeruginosa peritonitis.

Anti-Bacterial Agents↗
PubMed1986

Comparative evaluation of ciprofloxacin, enoxacin, and ofloxacin in experimental Pseudomonas aeruginosa pneumonia.

The therapeutic activity of ciprofloxacin, enoxacin, and ofloxacin was evaluated in guinea pigs with acute and chronic experimental Pseudomonas aeruginosa pneumonia. Intratracheal instillations of P. aeruginosa resulted in fatal pneumonia in all untreated animals within 36 h. Among treatment groups (80 mg/kg [body weight] per day), cumulative survival rates were: 47%, ciprofloxacin; 55%, enoxacin; and 42%, ofloxacin. These rates were not significantly different. Intrapulmonary killing of P. aeruginosa was equivalent 3 h after a single dose of ciprofloxacin or ofloxacin (20 mg/kg) or enoxacin (40 mg/kg). The combination of ciprofloxacin with azlocillin, ceftazidime, or tobramycin did not increase the efficacy of intrapulmonary killing of P. aeruginosa over that of ciprofloxacin alone. A chronic, nonfatal bronchopneumonia was induced in guinea pigs by intratracheal instillation of microscopic agar beads impregnated with a mucoid strain of P. aeruginosa. Compared with no treatment, ciprofloxacin and enoxacin produced greater than or equal to 99.9% intrapulmonary killing, and ofloxacin sterilized the lungs completely, after 4 days of treatment. In no quinolone-treated animal did resistant strains of P. aeruginosa emerge during 4-day treatment periods. In further studies with the chronic model, oral and parenteral ciprofloxacin treatment were found to be equivalent in efficacy. We conclude that several quinolone derivatives may be effective for the treatment of P. aeruginosa pneumonia and that combinations of quinolones with beta-lactams or aminoglycosides may not increase efficacy against P. aeruginosa pneumonia.

Animals↗
PubMed1986

Comparative activities of the beta-lactamase inhibitors YTR 830, clavulanate, and sulbactam combined with ampicillin and broad-spectrum penicillins against defined beta-lactamase-producing aerobic gram-negative bacilli.

The in vitro synergistic activities of the beta-lactamase inhibitors YTR 830, clavulanate, and sulbactam, combined with ampicillin, ticarcillin, mezlocillin, azlocillin, piperacillin, and apalcillin, were determined against 34 strains of members of the Enterobacteriaceae family, Pseudomonas aeruginosa, Aeromonas hydrophila, and Haemophilus influenzae with characterized plasmid or chromosomal beta-lactamases or both. Strains were tested against fixed concentrations of beta-lactamase inhibitors (8 micrograms/ml) combined with doubling dilutions of beta-lactams. Synergy was defined as a fourfold or greater decrease in the MIC of the beta-lactam. Against Enterobacteriaceae producing Richmond and Sykes class III and V plasmid-mediated beta-lactamases, synergy was obtained against most strains with YTR 830- and clavulanate-beta-lactam combinations, with sulbactam being less effective. Against Enterobacteriaceae producing class I chromosomal beta-lactamases, combinations containing YTR 830 or sulbactam were more synergistic than combinations containing clavulanate. Against strains producing class V PSE enzymes, all three inhibitors were synergistic with piperacillin and apalcillin against strains producing PSE-1, -3, and -4 enzymes, while the PSE-2-producing strain was resistant to all inhibitors. YTR 830-beta-lactam combinations were also synergistic against strains producing the novel beta-lactamases OHIO-1, TLE-1, AER-1, and ROB-1. Overall, YTR 830 with piperacillin or apalcillin was the most effective combination.

Ampicillin↗
PubMed1987

Broth microdilution testing of susceptibilities to 30 antimicrobial agents of Mycobacterium avium strains from patients with acquired immune deficiency syndrome.

A total of 31 strains of Mycobacterium avium complex isolated from patients with acquired immune deficiency syndrome were tested for susceptibility to 30 antimicrobial agents by using microdilution trays containing dried antimicrobial agents. MICs were determined over a period of 7 days of growth in a broth medium (7HSF) that is equivalent to 7H11 agar. MICs obtained by this method showed good agreement with MICs determined by the agar dilution method. Strains could be divided into two groups by their antimicrobial susceptibility patterns. All group 1 strains (8 of the 31 strains tested) were at least moderately susceptible to inhibition by a variety of beta-lactam antimicrobial agents, including amoxicillin-clavulanic acid and cefmenoxime. Group 2 strains (23 of 31) were susceptible only to amikacin (22 of 23 strains). All 31 strains were resistant to oxacillin, clindamycin, erythromycin, tetracycline, chloramphenicol, vancomycin, nitrofurantoin, and aztreonam at the highest concentration of antimicrobial agent present in the microdilution trays. The addition of Tween 80 to 7HSF broth increased the susceptibility of M. avium complex to many of the antimicrobial agents tested. Killing of M. avium complex (i.e., less than or equal to 1% survival after 7 days) was found to vary for different strains and antimicrobial agents. Killing of some strains by amoxicillin-clavulanic acid, carbenicillin, azlocillin, cefmenoxime, cefotaxime, amikacin, and ampicillin occurred at concentrations of antimicrobial agent that are achievable in serum. Further studies are needed to determine whether any of these antimicrobial agents has activity against M. avium complex cells that have been ingested by macrophages.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Isolation and characterization of a penicillinase from Pseudomonas cepacia 249.

Pseudomonas cepacia has an inducible beta-lactamase which is responsible for its novel ability to catabolize beta-lactam compounds. The gene encoding this enzyme, penA, was cloned from a genomic library of P. cepacia 249 on the broad-host-range cosmid pLAFR. This separated the penA gene from the gene encoding a second beta-lactamase in P. cepacia 249. Expression of penA was inducible in an Escherichia coli host strain by low levels of penicillin. The 33,500-molecular-weight enzyme had penicillinase activity not inhibited by clavulanic acid or sulbactam and was highly active against piperacillin and azlocillin. In comparison with other inducible beta-lactamases produced by gram-negative organisms, the penA enzyme had many properties which were similar to those of the penicillinase produced by Alcaligenes faecalis. It was unlike the ampC-type cephalosporinase produced by Pseudomonas aeruginosa.

Cloning, Molecular↗
PubMed1989

Reactivation of peptidoglycan synthesis in ether-permeabilized Escherichia coli after inhibition by beta-lactam antibiotics.

The recovery of peptidoglycan-synthesizing activity after inhibition by beta-lactam antibiotics was investigated in ether-permeabilized cells of Escherichia coli B. Such cells synthesize sodium dodecyl sulfate-insoluble peptidoglycan when provided with UDP-linked precursors and Mg2+. The ability of beta-lactam antibiotics to inhibit the synthesis of peptidoglycan was correlated with their affinity for penicillin-binding proteins 1A and 1Bs. Penicillin-binding protein 1Bs is thought to be the major peptidoglycan synthetase in E. coli and is a major lethal target for beta-lactam antibiotics. Ether-treated bacteria were preincubated with concentrations of beta-lactams sufficient to completely inhibit peptidoglycan synthesis and then treated with beta-lactamases to inactivate free antibiotic prior to measurement of peptidoglycan synthesis. At 40 min after beta-lactamase treatment, the rate of peptidoglycan synthesis was about 74% of the control rate in cells pretreated with ampicillin, but only 15% of the control in cells pretreated with penicillin G or azlocillin. Reversal of inhibition by several other antibiotics fell between these extremes. When cross-linking of peptidoglycan was measured specifically, reversal of inhibition by ampicillin also occurred more readily than that by penicillin G. Reactivation of peptidoglycan synthesis was not due to de novo synthesis of penicillin-binding proteins since it occurred under conditions that did not allow incorporation of [14C]leucine. We conclude that there is considerable variation in the stability of the inactive acyl enzymes formed between various beta-lactams and penicillin-binding protein 1Bs, with those formed by penicillin G being relatively long-lived.

Anti-Bacterial Agents↗
PubMed1990

Cross resistance to ciprofloxacin and other antimicrobial agents among clinical isolates of Acinetobacter calcoaceticus biovar anitratus.

Using an agar dilution assay, for 66 of 104 (63.5%) clinical isolates of Acinetobacter calcoaceticus biovar anitratus, the MIC of ciprofloxacin was greater than or equal to 1.0 micrograms/ml. Cross resistance was demonstrable to ciprofloxacin and gentamicin (P less than 0.001), amikacin (P less than 0.01), cefotaxime (P less than 0.001), azlocillin (P less than 0.001), ceftazidime (P less than 0.001), trimethoprim-sulfamethoxazole (P less than 0.001), and minocycline (P less than 0.05). The mean MIC of ciprofloxacin for drug-susceptible isolates was consistently lower than that for resistant isolates; however, these differences were significant only for amikacin (P = 0.036).

Acinetobacter↗
PubMed1993

Activities of potential therapeutic and prophylactic antibiotics against blood culture isolates of viridans group streptococci from neutropenic patients receiving ciprofloxacin.

All 47 sequential blood culture isolates of viridans group streptococci obtained from febrile neutropenic patients receiving quinolone prophylaxis were susceptible to vancomycin, teicoplanin, and imipenem. Resistance to benzylpenicillin (MIC for 50% of isolates [MIC50], 0.125 microgram/ml) and ceftazidime (MIC50, 4 micrograms/ml) was common. Most isolates were susceptible to amoxicillin, co-amoxiclav (amoxicillin-clavulanic acid at a 2:1 ratio by weight), azlocillin, clarithromycin, and erythromycin, with azithromycin showing comparable activity. The MIC90 of sparfloxacin was 1 microgram/ml; those for ciprofloxacin and ofloxacin were > 16 and 16 micrograms/ml, respectively.

Anti-Bacterial Agents↗
PubMed1998

Recombinant expression and characterization of the major beta-lactamase of Mycobacterium tuberculosis.

New antibiotic regimens are needed for the treatment of multidrug-resistant tuberculosis. Mycobacterium tuberculosis has a thick peptidoglycan layer, and the penicillin-binding proteins involved in its biosynthesis are inhibited by clinically relevant concentrations of beta-lactam antibiotics. beta-Lactamase production appears to be the major mechanism by which M. tuberculosis expresses beta-lactam resistance. beta-Lactamases from the broth supernatant of 3- to 4-week-old cultures of M. tuberculosis H37Ra were partially purified by sequential gel filtration chromatography and chromatofocusing. Three peaks of beta-lactamase activity with pI values of 5.1, 4.9, and 4.5, respectively, and which accounted for 10, 78, and 12% of the total postchromatofocusing beta-lactamase activity, respectively, were identified. The beta-lactamases with pI values of 5.1 and 4.9 were kinetically indistinguishable and exhibited predominant penicillinase activity. In contrast, the beta-lactamase with a pI value of 4.5 showed relatively greater cephalosporinase activity. An open reading frame in cosmid Y49 of the DNA library of M. tuberculosis H37Rv with homology to known class A beta-lactamases was amplified from chromosomal DNA of M. tuberculosis H37Ra by PCR and was overexpressed in Escherichia coli. The recombinant enzyme was kinetically similar to the pI 5.1 and 4.9 enzymes purified directly from M. tuberculosis. It exhibited predominant penicillinase activity and was especially active against azlocillin. It was inhibited by clavulanic acid and m-aminophenylboronic acid but not by EDTA. We conclude that the major beta-lactamase of M. tuberculosis is a class A beta-lactamase with predominant penicillinase activity. A second, minor beta-lactamase with relatively greater cephalosporinase activity is also present.

Drug Resistance, Multiple↗
PubMed1999

Activities of beta-lactams and macrolides against Helicobacter pylori.

A continuous-culture system (chemostat) was used to study the activities of beta-lactam antimicrobial agents, clarithromycin, and 14-OH-clarithromycin against slowly growing Helicobacter pylori NCTC 11637. H. pylori was grown to steady state before exposure to these antimicrobial agents at x8 the MIC. The bactericidal actions of combinations of amoxicillin and clarithromycin were also studied. Viable counts (numbers of CFU per milliliter) were determined at 2-h intervals for 12 h and at 20 h after the addition of antibiotics. The effects of pH changes (6.5 to 7.4) on the activities of amoxicillin, clarithromycin, and the combination of these against H. pylori NCTC 11637 were also studied. Viable counts following exposure to ampicillin, cefixime, ceftazidime, cefuroxime, cefotaxime, azlocillin, and piperacillin at 20 h showed bacteriostatic activity. Imipenem, meropenem, amoxicillin, clarithromycin, and 14-OH-clarithromycin reduced the viable counts by 3 log10 CFU/ml (>/=99.9% killing). Imipenem was the most rapidly bactericidal against H. pylori NCTC 11637. Results of the pH experiments showed that amoxicillin was bactericidal at pHs 6.5 to 7. 4. Clarithromycin was bactericidal at pH 7.0 to 7.4 but was bacteriostatic at pH 6.5. The combination of amoxicillin and clarithromycin was bactericidal at pHs 6.5 and 7.0. A batch culture (flask system) was also used to investigate 12 strains of H. pylori for their susceptibilities to beta-lactams, clarithromycin, and/or 14-OH-clarithromycin in order to determine whether results from the chemostat model can be reproduced with batch cultures. Results of the chemostat time-kill kinetic study were reproducible in our batch culture flask system. The role of carbapenems in the eradication of H. pylori should be investigated.

Anti-Bacterial Agents↗
PubMed2000

Purification and biochemical characterization of the VIM-1 metallo-beta-lactamase.

VIM-1 is a new group 3 metallo-beta-lactamase recently detected in carbapenem-resistant nosocomial isolates of Pseudomonas aeruginosa from the Mediterranean area. In this work, VIM-1 was purified from an Escherichia coli strain carrying the cloned bla(VIM-1) gene by means of an anion-exchange chromatography step followed by a gel permeation chromatography step. The purified enzyme exhibited a molecular mass of 26 kDa in sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and an acidic pI of 5.1 in analytical isoelectric focusing. Amino-terminal sequencing showed that mature VIM-1 results from the removal of a 26-amino-acid signal peptide from the precursor. VIM-1 hydrolyzes a broad array of beta-lactam compounds, including penicillins, narrow- to expanded-spectrum cephalosporins, carbapenems, and mechanism-based serine-beta-lactamase inactivators. Only monobactams escape hydrolysis. The highest catalytic constant/K(m) ratios (>10(6) M(-1). s(-1)) were observed with carbenicillin, azlocillin, some cephalosporins (cephaloridine, cephalothin, cefuroxime, cefepime, and cefpirome), imipenem, and biapenem. Kinetic parameters showed remarkable variability with different beta-lactams and also within the various penam, cephem, and carbapenem compounds, resulting in no clear preference of the enzyme for any of these beta-lactam subfamilies. Significant differences were observed with some substrates between the kinetic parameters of VIM-1 and those of other metallo-beta-lactamases. Inactivation assays carried out with various chelating agents (EDTA, 1,10-o-phenanthroline, and pyridine-2,6-dicarboxylic acid) indicated that formation of a ternary enzyme-metal-chelator complex precedes metal removal from the zinc center of the protein and revealed notable differences in the inactivation parameters of VIM-1 with different agents.

Anti-Bacterial Agents↗
PubMed2002

Comparative stability studies of antipseudomonal beta-lactams for potential administration through portable elastomeric pumps (home therapy for cystic fibrosis patients) and motor-operated syringes (intensive care units).

The stability of antipseudomonal beta-lactams in concentrated solutions was examined in view of their potential administration by continuous infusion with external pumps (for intensive care patients) or with portable pumps carried under clothing (for cystic fibrosis patients). Aztreonam (100 g/liter), piperacillin (128 g/liter, with tazobactam), and azlocillin (128 g/liter) remained 90% stable for up to more than 24 h at 37 degrees C (mezlocillin [128 g/liter] was stable at 25 degrees C but not at 37 degrees C). Ceftazidime (120 g/liter), cefpirome (32 g/liter), and cefepime (50 g/liter) remained 90% stable for up to 24, 23.7, and 20.5 h at 25 degrees C but only for 8, 7.25, and 13 h at 37 degrees C, respectively. The control of temperature therefore appears to be critical for all three cephalosporins that cannot be recommended for use in portable pumps carried under clothes for prolonged periods for reasons of stability. Cefpirome and cefepime solutions developed an important color change (from light yellow to dark red) upon exposure when stored at 30 degrees C or higher. Degradation of ceftazidime was accompanied by the liberation of pyridine which, at 37 degrees C, was in excess of what is allowed by the U.S. Pharmacopeia, i.e., 1.1 mg/liter, after 8 and 12 h for drug concentrations of 12 and 8.3%, respectively. Imipenem and meropenem are too unstable (10% degradation at 25 degrees C after 3.5 and 5.15 h, respectively) to be recommended for use by continuous infusion. Faropenem, examined in comparison with imipenem and meropenem, proved as stable as aztreonam or piperacillin.

Anti-Bacterial Agents↗
PubMed2004

Molecular characterization of a beta-lactamase gene, blaGIM-1, encoding a new subclass of metallo-beta-lactamase.

As part of the SENTRY Antimicrobial Surveillance Program in 2002, five multidrug-resistant Pseudomonas aeruginosa clinical isolates were detected with metallo-beta-lactamase (MbetaL) activity. The isolates were recovered from different patients in a medical center located in Dusseldorf, Germany. The resistant determinant was isolated amplifying the region between the integrase and the aacA4 gene cassette. Sequencing revealed a novel MbetaL gene, designated bla(GIM-1). Additional analysis showed that GIM-1, comprising 250 amino acids and with a pI value of 5.4, differs in its primary sequence from that described for IMP, VIM, and SPM-1 enzymes by 39 to 43%, 28 to 31%, and 28%, respectively. The enzyme possesses unique amino acids within the major consensus sequence (HXHXD) of the MbetaL family. Kinetics analysis revealed that GIM-1 has no clear preference for any substrate and did not hydrolyze azlocillin, aztreonam, and the serine-beta-lactamase inhibitors. bla(GIM-1) was found on a 22-kb nontransferable plasmid. The new MbetaL gene was embedded in the first position of a 6-kb class 1 integron, In77, with distinct features, including an aacA4 cassette downstream of the MbetaL gene that appeared to be truncated with bla(GIM-1). The aacA4 was followed by an aadA1 gene cassette that was interrupted by a copy of the IS1394. This integron also carried an oxacillinase gene, bla(OXA-2), before the 3'-CS region. GIM-1 appears to be a unique MbetaL, which is located in a distinct integron structure, and represents the fourth subclass of mobile MbetaL enzymes to be characterized.

Amino Acid Sequence↗
PubMed1985

Effects of storage temperature and pH on the stability of eleven beta-lactam antibiotics in MIC trays.

Microdilution MIC test trays containing 11 beta-lactam antibiotics in Mueller-Hinton broth at pH 7.31 or 6.80 were prepared and stored at 4, -10, -25, and -70 degrees C. The drugs tested were ampicillin, ticarcillin, mezlocillin, piperacillin, azlocillin, cefazolin, cefotaxime, moxalactam, cefoperazone, ceftriaxone, and imipenem. MICs for Staphylococcus aureus ATCC 29213, Escherichia coli ATCC 25922, and Pseudomonas aeruginosa ATCC 27853 were determined at weekly intervals for up to 1 year. The data from the MIC determinations showed the stability of antimicrobial activity over time to be -70 degrees C greater than -25 degrees C approximately 4 degrees C much greater than -10 degrees C. The relative stability at 4 degrees C as compared with that at -10 degrees C cannot be explained by desiccation, as determined by changes in broth sodium concentrations. The relative instability at -10 degrees C may have been caused in part by a temperature fluctuation, resulting in intermittent freezing and thawing of the antibiotics. Some of the drugs appeared to be more stable when diluted in broth at pH 6.80, but endpoints were more difficult to read. Cefazolin and cefoperazone were stable at all four storage temperatures. Cefotaxime, moxalactam, and ceftriaxone also were relatively stable. The other drugs showed moderately rapid to rapid deterioration at each temperature except -70 degrees C. Storage at -25 degrees C is suitable for up to 3 months for many, but not all, beta-lactams; -10 degrees C appears to be unsuitable. Storage at -70 degrees C is recommended.

Anti-Bacterial Agents↗
PubMed1989

Oropharyngeal and fecal carriage of Pseudomonas aeruginosa in hospital patients.

This prospective study was designed to determine the incidence of rectal and/or oropharyngeal colonization rates of patients with Pseudomonas aeruginosa upon admission to a general hospital and the risk of becoming colonized while hospitalized. Consecutive 186 admissions (180 patients) to one medical ward, one surgical ward, and the intensive care unit were studied over a period of 5 months. Rectal and oropharyngeal swabs for P. aeruginosa were obtained on admission, weekly thereafter, and/or upon discharge. Forty-two patients (22.6%) were colonized on admission, 20 patients (10.8%) acquired P. aeruginosa during hospitalization. Colonization on admission was observed twice as frequently on the surgical ward and in the intensive care unit as on the medical ward. Positive rectal cultures were more frequent than oropharyngeal cultures throughout the study (P less than 0.01). For patients admitted culture positive or culture negative, the probabilities of remaining culture positive or culture negative, respectively, remained at 44 and 72% after 35 days of hospitalization. The most common P. aeruginosa serotypes were 1, 6, and 10, and pyocin types 1, 3, and 10 were predominant. There was no statistical difference in the serotypes or pyocin types detected on admission or acquired during hospitalization. Except for two hospital-acquired first isolates which were resistant to moxalactam, all first isolates were susceptible to the four antibiotics tested. During the study, one isolate became resistant to azlocillin, gentamicin, and tobramycin, while two isolates became resistant to moxalactam. A statistical analysis was performed for 13 risk factors for all colonized and noncolonized patients. Colonization detected at the time admission was positively associated with age ( > 65 years), previous surgery of the gastrointestinal tract for neoplasm, and anemia ( P< 0.05). In contrast, for patients who entered the study culture negative, none of the analyzed 13 risk factors was associated with an increased probability for colonization. This observation included the administration of antimicrobial agents singly or in combination or both.

Carrier State↗
PubMed1989

Epidemic Pseudomonas aeruginosa serotype O16 bacteremia in hematology-oncology patients.

From 1 August 1978 through 31 December 1982, 98 hematology-oncology patients had positive cultures for Pseudomonas aeruginosa serotype O16; 22 of these patients developed bacteremia, and this bacteremia was associated with the occurrence of extensive perineal cellulitis in 10 patients (45.5%). Seventeen bacteremic patients died. The epidemic strain differed from other P. aeruginosa organisms isolated at the hospital by its resistance to all antibiotics available at that time (ticarcillin, piperacillin, azlocillin, tobramycin, ceftizoxime, ceftriaxone, moxalactam, ceftazidime, and fosfomycin). Univariate analysis showed the following factors to be significantly associated with P. aeruginosa O16 bacteremia: the severity of granulocytopenia at the time of the bacteremia, more days with fever, the administration of ticarcillin or an aminoglycoside, the receipt of a greater number of antimicrobial agents for a longer period of time before documentation of the bacteremia, and the occurrence of cellulitis. Logistic regression analysis showed that duration of fever, duration of bacteremia, and the number of antimicrobial agents administered before documentation of the bacteremia were the best predictors of P. aeruginosa O16 bacteremia. In a prospective study of the acquisition of P. aeruginosa by hematology-oncology patients, 1,149 specimens (throat and rectal swabs) from 270 patients and 201 specimens from their washbasin drains were collected. On only three occasions was the epidemic strain isolated from both the patient and his or her washbasin, but in each case the colonization of the patient preceded the isolation of the strain from the washbasin. The transmission of any P. aeruginosa organism from washbasin drain to patient could not be documented. Contact isolation precautions from the Centers for Disease Control were used for all hematology-oncology patients colonized or infected with P. aeruginosa after 7 January 1983. No case of P. aeruginosa O16 bacteremia has occurred at Hotel Dieu since July 1984.

Adult↗