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PubMed1989

The beige mouse model for Mycobacterium avium complex (MAC) disease: optimal conditions for the host and parasite.

We extended our earlier studies to establish the beige (C57B1/6/bgJ/bgJ) mouse model for experimental acute infections with Mycobacterium avium complex (MAC). Optimal conditions of the host and the parasites have been determined. Mice bred at our center showed similar responses to those obtained from Jackson Laboratories, the original supplier. Both male and female mice showed similar responses, but older mice in both sexes showed less susceptibility than younger mice. Strain 101 of MAC showed remarkable consistency in its pathogenicity to beige mice, as evidenced by the distribution of colony forming unit (CFU) counts at various time points after intravenous challenge, in several experiments. CFU counts showed an association with the dose of challenge, and histopathological observations.

Animals↗
PubMed1995

Comparative anti-HIV evaluation of diverse HIV-1-specific reverse transcriptase inhibitor-resistant virus isolates demonstrates the existence of distinct phenotypic subgroups.

We have biologically and biochemically evaluated a structurally diverse group of HIV-1-specific reverse transcriptase (RT) inhibitors and determined that the members of this class share many common properties. These include reproducible and selective antiviral activity against a panel of biologically distinct laboratory and clinical strains of HIV-1, activity against HIV-1 in a wide variety of cultured and fresh human cells, and potent inhibition of HIV-1 RT when evaluated using a heteropolymeric ribosomal RNA template assay. Each of the HIV-1-specific compounds was capable of inhibiting HIV replication when challenged at high m.o.i., further distinguishing them from the nucleoside analogs 3'-azido-3'-deoxythymidine (AZT) and 2',3'-dideoxycytidine (ddC). When tested in combination with AZT, each of the HIV-1-specific compounds synergistically inhibited the replication of HIV-1. HIV-1 isolates resistant to different HIV-1-specific inhibitors exhibited heterogeneous patterns of cross-resistance to other members of this pharmacologic class. Four distinct phenotypic classes have been defined through the use of drug-resistant virus isolates which derive from distinct mutations in the RT. These results indicate that the various subgroups of HIV-1-specific inhibitors interact differently with HIV-1 RT, suggesting important potential implications for drug combination therapeutic strategies.

Antiviral Agents↗
PubMed1988

Antigenicity and immunogenicity of Hypoderma lineatum soluble proteins in the bovine host.

Protein species found in soluble crude extracts of Hypoderma lineatum (common cattle grub) 1st-instar larvae (HL1) were separated by non-denaturing and denaturing polyacrylamide gel electrophoresis (PAGE) and analyzed for antigenicity by Western blotting using serum from H. lineatum-infested and vaccinated cattle. All HL1 proteins resolved by non-denaturing PAGE were found to be antigenic in the infested bovine host. Treatment of the proteins with sodium dodecyl sulfate and 2-mercaptoethanol destroyed the ability of hypodermin B and the Peak 2 proteins from DEAE-ion exchange HPLC to be bound by antibody. The principal proteins, hypodermin A and hypodermin C (collagenase), appear to be the most immunogenic of the larval proteins. Although having similar amino acid composition, hypodermin A did not appear to share an antigenic epitope with the most prevalent protein, hypodermin C. These results may allow for the selection of proteins to be used in vaccine trials and studies of protective immunological mechanisms associated with acquired resistance to H. lineatum infestation in the bovine host.

Animals↗
PubMed1992

Does high level production of SHV-type penicillinase confer resistance to ceftazidime in Enterobacteriaceae?

We report the isolation of a clinical isolate of Klebsiella pneumoniae that showed resistance to ceftazidime (MIC: 8 micrograms/ml), susceptibility to aztreonam (MIC: 2 micrograms/ml) and cefotaxime (MIC: 0.015 micrograms/ml). A synergistic effect between clavulanic acid and ceftazidime or aztreonam against this strain was also observed. The strain hyperproduced SHV-1 penicillinase (990 U/g) which is encoded by a self-transferrable plasmid of at least 150 kb. That the ceftazidime-resistance phenotype could be due to hyperproduction of SHV-1 penicillinase is supported by the study of a spontaneous ceftazidime-resistant mutant in vitro obtained from an Escherichia coli strain containing plasmid p453 encoding the SHV-1. Indeed, this mutant hyperproducing SHV-1 (2200 U/g) was resistant to ceftazidime (MIC: 16 micrograms/ml) and aztreonam (MIC: 8 micrograms/ml) but susceptible to cefotaxime (MIC: 0.03 ng/ml). Clavulanic acid showed a synergistic effect when associated with ceftazidime or aztreonam. In contrast, the hyperproduction of TEM-1 (790 U/g) did not confer a ceftazidime- and aztreonam-resistant phenotype while hyperproduction of both TEM-1 and SHV-1 increased the resistance to amoxycillin/clavulanic acid and to cephalothin.

Ceftazidime↗
PubMed1994

Attenuation of gentamicin ototoxicity by glutathione in the guinea pig in vivo.

The effect of glutathione co-therapy on the expression of gentamicin ototoxicity was tested in pigmented guinea pigs. The first group of animals was injected with gentamicin (100 mg/kg body weight/day) for two weeks followed by 10 weeks of rest. A second group received glutathione by gastric gavage immediately prior to each gentamicin injection. Two groups of controls were treated either with saline injections or glutathione gavage alone. Auditory brainstem responses, taken at 2-week intervals, revealed a progressive gentamicin-induced hearing loss reaching a 30 to 40 dB threshold shift at 2 kHz, approximately 60 dB at 8 kHz and 80 dB at 18 kHz. Glutathione co-therapy slowed the progression of hearing loss and significantly attenuated the final threshold shifts by 20 to 40 dB. Morphological evaluation confirmed hair cell loss after gentamicin treatment and protection by glutathione. Drug serum levels were assayed at 2 and 7 days of treatment. There were no differences between the gentamicin (mean = 183 micrograms/ml; range, 90 to 300) and the gentamicin/glutathione group (mean = 164 micrograms/ml; range, 80 to 320). Antimicrobial activity of gentamicin was tested against Staphylococcus aureus and Pseudomonas aeruginosa. A 30-fold molar excess of glutathione did not influence the efficacy of gentamicin. These studies suggest that glutathione protects against ototoxicity by interfering with the cytotoxic mechanism.

Animals↗
PubMed1984

Unpredictable interactions between cefotetan and penicillins or aminoglycosides.

The bacteriostatic and bactericidal activity of gentamicin, amikacin, piperacillin, azlocillin, ampicillin, benzyl penicillin, and oxacillin against 85 selected isolates was measured alone and in the presence of subinhibitory concentrations of cefotetan. A potential for antagonistic interactions between cefotetan and acylamino penicillins (piperacillin greater than azlocillin greater than ampicillin) were observed with some strains; synergy was suggested with other isolates, however, Bacteriostatic and bactericidal activity of the two aminoglycosides was enhanced by cefotetan with most gram-negative bacilli, but bactericidal activity was significantly diminished with 4 of 65 strains. Piperacillin and cefotetan were clearly antagonistic with 11 of 44 strains and synergistic with 4 of 44 strains of gram-negative bacilli: the remaining 21 strains gave off scale end points and could not be analyzed in that way.

Aminoglycosides↗
PubMedDate not supplied

Resistance of Xanthomonas maltophilia to antibiotics and the effect of beta-lactamase inhibitors.

We examined the susceptibility of 50 isolates of Xanthomonas maltophilia and the effect of beta-lactamase inhibitors upon the susceptibility. The majority of isolates were resistant to azlocillin, piperacillin, mezlocillin, ticarcillin, cefotaxime, ceftizoxime, ceftriaxone, cefoperazone, and ceftazidime. All isolates were resistant to imipenem, CGP 31608, aztreonam, and carumonam. Although disk susceptibility tests showed that the combination of clavulanate with ticarcillin inhibited many isolates, at a ratio of 1:20 few isolates were susceptible to the combination. Addition of clavulanate to aztreonam and to imipenem failed to make organisms susceptible. Sulbactam combined with cefoperazone made some organisms susceptible, but ampicillin-sulbactam was ineffective, whereas tazobactam combined with piperacillin at a ratio of 1:4 made half the isolates have MICs of 32 micrograms/ml or less. The beta-lactamases from the isolates hydrolyzed all of the beta-lactams.

Anti-Bacterial Agents↗
PubMedDate not supplied

Comparative in vitro activity of cefoperazone and various combinations of cefoperazone/sulbactam.

Cefoperazone with 2 and 4 micrograms/ml of sulbactam and in a 2:1 ratio was tested against 1258 clinical isolates of Gram-positive and Gram-negative bacteria, as well as against Gram-negative bacilli that had stably derepressed Type I beta-lactamase or that were hyperproductive of non-Type I beta-lactamases. The 2:1 cefoperazone/sulbactam combination was the most potent combination tested. With this combination cefoperazone minimum inhibitory concentrations (MICs) of 27 of 40 (67%) of the clinical isolates of Pseudomonas species and 64 of 67 (95%) of clinical isolates of the Enterobacteriaceae were reduced from greater than or equal to 64 micrograms/ml by at least two-fold. In contrast, cefoperazone MICs of greater than or equal to 64 micrograms/ml remained unchanged for 26 (65%) and 24 (60%) of Pseudomonas species and 35 (52%) and 30 (45%) of the Enterobacteriaceae in the presence of 2 and 4 micrograms/ml of sulbactam, respectively. Cefoperazone/sulbactam in the 2:1 ratio was also the most active combination against the mutants derepressed for Type I beta-lactamase. Although the 2:1 combination of cefoperazone/sulbactam had the greatest potency in vitro, it remains to be seen whether this combination is predictive of clinical outcome from treatment of cefoperazone-resistant Gram-negative bacilli with cefoperazone/sulbactam.

Bacteria↗
PubMedDate not supplied

In vitro activity of cefoperazone/sulbactam and other antimicrobials against anaerobic bacteria.

Sulbactam inhibits the hydrolytic activity of several, clinically important beta-lactamases including those produced by anaerobic bacteria. This study was undertaken to determine the effect of sulbactam on the activity of cefoperazone against 250 anaerobic bacteria including 174 isolates belonging to the Bacteroides fragilis group and to compare the activity of cefoperazone/sulbactam with other antimicrobial agents. beta-lactamase activity was detected in 98% of the isolates of the Bacteroides fragilis group but not in the other species evaluated. Antagonistic activity between cefoperazone and sulbactam was not observed with any of the species. Forty-two percent of the isolates belonging to the B. fragilis group were resistant to cefoperazone. Ninety-four percent of these were converted to either the susceptible or moderately susceptible range upon the addition of sulbactam. Sixty-seven percent were susceptible to the combination cefoperazone/sulbactam and 27% were moderately susceptible. Overall, metronidazole and chloramphenicol were the most active antimicrobials. Significant differences in the antimicrobial susceptibility patterns of members of the B. fragilis group were observed. Sulbactam demonstrated some intrinsic activity against all of the species tested.

Anti-Bacterial Agents↗
PubMedDate not supplied

The bactericidal activity of ampicillin, daptomycin, and vancomycin against ampicillin-resistant Enterococcus faecium.

Ampicillin, daptomycin, and vancomycin, alone and in combination with gentamicin, were examined for bactericidal effects on ampicillin-resistant Enterococcus faecium using broth dilution minimum inhibitory concentrations (MICs) and time-kill studies. We tested 12 ampicillin-resistant isolates and demonstrated the following MICs and MBCs, respectively: ampicillin, greater than or equal to 32 micrograms/ml and greater than 256 micrograms/ml; daptomycin, less than or equal to 4 micrograms/ml and less than or equal to 16 micrograms/ml; and vancomycin, less than or equal to 4 micrograms/ml and greater than 64 micrograms/ml. Time-kill studies demonstrated that daptomycin alone had marked activity against the ampicillin-resistant E. faecium and that the addition of gentamicin resulted in synergistic killing. In addition, ampicillin and vancomycin were not bactericidal for the ampicillin-resistant isolates without the addition of gentamicin. The present study supports the consideration of daptomycin alone or in combination with an aminoglycoside as an alternative therapy for ampicillin-resistant enterococci, although additional clinical experience is now necessary.

Ampicillin↗
PubMed1994

Laboratory diagnosis of oxacillin resistance in Staphylococcus aureus by a multiplex-polymerase chain reaction assay.

A polymerase chain reaction (PCR) test was developed in which the mecA gene responsible for the intrinsic resistance to oxacillin in Staphylococcus aureus and the gyrA gene, always present in this species, were amplified in one operation. Among the 468 clinical isolates tested, the results obtained for 454 of the isolates (97%) were consistent with those of MIC determination. Discrepant results were noted for strains with low-level oxacillin resistance (MICs, 4-8 micrograms/ml) and mecA gene negative. For these strains, susceptibility to oxacillin was restored in the presence of a beta-lactamase inhibitor, which suggested a resistance by penicillinase hyperproduction. In contrast, all of the high-level resistant strains (MICs, > 8 micrograms/ml) carried the mecA gene. The presence of this gene has frequently been associated with resistance to gentamicin, tetracycline, erythromycin, lincomycin, and pefloxacin. The PCR assay described in this study can be accomplished with ease and total confidence in the clinical microbiologic laboratory for a rapid and effective establishment of antistaphylococcal chemotherapy.

Bacterial Proteins↗
PubMed1995

Influence of beta-lactamase inhibitors on the activity of oxacillin against methicillin-resistant Staphylococcus aureus.

We studied the in vitro susceptibility to oxacillin of 46 isolates of methicillin-resistant Staphylococcus aureus (MRSA) isolates with a minimum inhibitory concentration (MIC) > 8 micrograms/ml of oxacillin, with and without adding clavulanic acid, sulbactam, or tazobactam in three different concentrations (2, 4, and 8 micrograms/ml). All 46 strains were found by the rapid chromogenic cephalosporin method to be beta-lactamase producers. For those strains with low-level resistance (MIC of 16 or 32 micrograms/ml), the MICs of oxacillin decreased four- to 32-fold and two- to 32-fold after adding sulbactam and tazobactam, respectively. For those with high-level resistance (MIC of > or = 64 micrograms/ml), the MICs either did not change or decreased only two-fold after we added one of three beta-lactamase inhibitors. The results suggest that beta-lactamase production probably plays a role in resistance to oxacillin in those MRSA strains of low-level oxacillin resistance.

Anti-Bacterial Agents↗
PubMed2006

Mendelian traits that confer predisposition or resistance to specific infections in humans.

Mutations in human genes involved in immunity are increasingly recognised. Most are associated with conventional primary immunodeficiencies, which confer Mendelian predisposition to multiple infectious diseases. Recently, there has been much study of monogenic traits that do not confer such a broad vulnerability. Defects in several genes confer predisposition to infection with specific bacteria and viruses in otherwise healthy individuals. Mutations in other genes even confer resistance to specific pathogens, with no detectable decrease in fitness. These 'experiments of nature' reveal surprising specific interactions between certain human genes and microbial pathogens.

Genetic Predisposition to Disease↗
PubMed2006

Delayed resistance selection for doripenem when passaging Pseudomonas aeruginosa isolates with doripenem plus an aminoglycoside.

Doripenem (formerly S-4661), a parenteral carbapenem, was tested in combination with an aminoglycoside (gentamicin) to determine the resistance selection of these codrugs during subinhibitory passaging using 6 Pseudomonas aeruginosa isolates. The organisms were selected based on doripenem and gentamicin MIC values to include isolates with MIC values near the susceptible breakpoints of both compounds and 1 strain highly resistant to gentamicin. Baseline MIC values were established for doripenem (2-8 microg/mL) and gentamicin (4 to >256 microg/mL) using reference broth microdilution methods, and passaging was carried out over 7 consecutive days. Doripenem MIC values increased 2 to >/=8-fold in 4 isolates, whereas 2 strains maintained the baseline doripenem MIC. When the experiment was performed with doripenem plus gentamicin, 3 strains maintained the original doripenem MIC values, 2 strains had a 2-fold increase, and only 1 strain showed a 4-fold increase in the doripenem MIC values. Previous studies have demonstrated doripenem to be more potent than other members in its class when tested against P. aeruginosa. The combination of doripenem and an aminoglycoside may be an effective treatment of infections caused by P. aeruginosa with elevated carbapenem MIC values with lower risk of selecting further resistance.

Aminoglycosides↗