Search PubMed⌕ Search

Biomedical subjects

M H Cynamon

Publications and source records attributed to M H Cynamon.

At least 55 records · Page 3Linked to original sources
PubMed1992

Activity of azithromycin against Mycobacterium avium infection in beige mice.

The comparative activities of azithromycin and clarithromycin and the activities of azithromycin alone and in combination with other antimycobacterial agents were evaluated in the beige mouse model of disseminated Mycobacterium avium complex infection. Azithromycin was similar in activity to clarithromycin. Azithromycin plus clofazimine plus ethambutol reduced the number of splenic organisms more than azithromycin alone, while the combination was less active than azithromycin alone for bacteria in lungs. Rifabutin had activity similar to that of azithromycin for organisms in spleens and lungs. Rifabutin plus azithromycin was more active than either agent alone for organisms in spleens, but the combination's activity was not significantly different from that of rifabutin for organisms in lungs. The activity of azithromycin against several M. avium complex isolates was evaluated. The reduction of viable cell counts in spleens ranged from 1.7 to 0.8 log units. For the three isolates studied, there was little correlation between the in vitro MIC and the in vivo activity.

Animals↗
PubMed1991

In vivo activities of newer rifamycin analogs against Mycobacterium avium infection.

The comparative activities of newer rifamycin analogs and the activity of rifabutin or rifapentine in combination with other antimycobacterial agents was evaluated in the beige (C57BL/6J; bgj/bgj) mouse model of disseminated Mycobacterium avium infection. Rifabutin and rifapentine at 20 mg/kg of body weight had comparable activities. P/DEA and CGP 7040 at 20 mg/kg were less active. The combination of ethambutol at 125 mg/kg and rifabutin at 20 mg/kg resulted in a slight increase in activity beyond that seen with rifabutin alone against organisms in the spleens. The combination of ethambutol and rifapentine at 20 mg/kg resulted in a modest increase in activity beyond that seen with rifapentine alone against organisms in the lungs. The combination of ethionamide at 125 mg/kg and rifapentine resulted in a decrease in activity compared with that for rifapentine alone. The combination of clofazimine at 20 mg/kg and rifapentine resulted in increased activity in the mouse model. The combination of clofazimine and rifapentine (or rifabutin) appears to be an attractive regimen that should be evaluated for the treatment of human infections due to M. avium complex.

Animals↗
PubMed1990

Liposome-encapsulated-gentamicin therapy of Mycobacterium avium complex infection in beige mice.

The efficacy of liposome-encapsulated gentamicin and free gentamicin was evaluated with the beige (C57BL/6J-bgj/bgj) mouse model of disseminated Mycobacterium avium complex infection. Approximately 10(7) viable M. avium complex cells were given intravenously. Seven days later, treatment with either encapsulated or free gentamicin at 20 mg/kg of body weight was started. Treatment was given daily for 5 consecutive days or twice weekly for 3 weeks. The mice were sacrificed 5 days after the last dose. Spleens, livers, and lungs were homogenized, and viable cell counts were determined. An analysis of variance and subsequent Tukey honestly significant difference tests indicated that both encapsulated and free gentamicin reduced viable cell counts in each of the organs compared with no treatment. Encapsulated gentamicin significantly reduced viable cell counts in the spleen and liver compared with the free gentamicin. A dose-response experiment was performed with a daily dose of 0.2, 2, or 20 mg/kg. Dose-related reductions in viable cell counts were observed for spleens and livers, although none of the regimens resulted in sterilization of these organs. Liposome-encapsulated gentamicin should be considered for further evaluation in the treatment of M. avium complex infection in humans.

Animals↗
PubMed1990

In vitro evaluation of nicotinamide riboside analogs against Haemophilus influenzae.

Exogenous NAD, nicotinamide mononucleotide, or nicotinamide riboside is required for the growth of Haemophilus influenzae. These compounds have been defined as the V-factor growth requirement. We have previously shown that the internalization of nicotinamide riboside is energy dependent and carrier mediated with saturation kinetics. Thionicotinamide riboside, 3-pyridinealdehyde riboside, 3-acetylpyridine riboside, and 3-aminopyridine riboside were prepared from their corresponding NAD analogs. These compounds and several other nicotinamide riboside analogs were evaluated for their ability to support the growth of H. influenzae and for their ability to block the uptake of [carbonyl-14C]nicotinamide riboside by H. influenzae. 3-Aminopyridine riboside blocked the uptake of [carbonyl-14C]nicotinamide riboside and inhibited the growth of H. influenzae when NAD, nicotinamide mononucleotide, or nicotinamide riboside served as the V factor. The antibacterial activity of 3-aminopyridine riboside was found to be specific for H. influenzae but had no effect on the growth of Staphylococcus aureus or Escherichia coli. In additional experiments by reversed-phase high-performance liquid chromatography, it was determined that whole cells of H. influenzae degrade 3-aminopyridine adenine dinucleotide to 3-aminopyridine riboside, which is then internalized. Inside the cell, 3-aminopyridine riboside has the ability to interfere with the growth of H. influenzae by an undetermined mechanism.

Chromatography, High Pressure Liquid↗
PubMed1989

Liposome-encapsulated-amikacin therapy of Mycobacterium avium complex infection in beige mice.

Efficacy of liposome-encapsulated amikacin and free amikacin against Mycobacterium avium complex was evaluated in the beige mouse (C57BL/6J-bgJ/bgJ) acute infection model. Approximately 10(7) viable M. avium complex serotype 1 cells for which the MIC of amikacin was 8 micrograms/ml were given intravenously. Treatment was started with encapsulated or free amikacin at approximately 110 or 40 mg/kg of body weight 7 or 14 days later. In the former experiment, treatment was given two or three times per week. In the latter experiment, treatment was given daily for 5 days. The animals were sacrificed 5 days after the last dose. Liver, spleen, and lung were homogenized, and viable cell counts were determined on 7H10 agar. An analysis of variance and subsequent Tukey HSD (honestly significant difference) tests indicated that both encapsulated and free amikacin significantly reduced viable cell counts in each of the organs compared with counts in the control group. Compared with free amikacin, encapsulated amikacin significantly reduced viable cell counts in the liver and spleen. Liposome encapsulation of an active agent appears to be a promising therapeutic approach to M. avium complex infection.

Amikacin↗
PubMed1989

New antimycobacterial agents.

Development of new antimycobacterial agents has gained impetus from the frequent occurrence of disseminated M. avium complex infections associated with the AIDS epidemic and the resurgence of tuberculosis. Promising new agents are being developed by modification of existing antimycobacterial agents (for example, aminoglycosides, macrolides, beta-lactams, and rifamycins) and by development of new therapeutic classes of drugs (for example, 4-quinolones). In addition, new drug delivery systems (liposome encapsulation) and immunomodulators may prove to be clinically useful in the treatment of some mycobacterial infections. New antimycobacterial agents will likely have their greatest impact on nontuberculous mycobacterial diseases because this is the area in which improved therapy is most needed. The specific role for new agents will be established only after more extensive study in animal models of mycobacterial infection is followed by controlled, randomized clinical trials.

Acquired Immunodeficiency Syndrome↗
PubMed1988

In-vitro susceptibility of Mycobacterium tuberculosis, Mycobacterium bovis and Mycobacterium kansasii to amoxycillin and ticarcillin in combination with clavulanic acid.

The in-vitro susceptibility of Mycobacterium tuberculosis, M. bovis, and M. kansasii to amoxycillin alone and in combination with 2 mg/l of clavulanic acid was evaluated by broth dilution. The MIC90 of amoxycillin plus clavulanic acid was 4 mg/l compared with greater than 32 mg/l for amoxycillin alone when tested against M. tuberculosis (n = 27). M. bovis (n = 8) was the most susceptible species with an MIC90 of amoxycillin 8 mg/l, compared with 0.5 mg/l for the combination. M. kansasii (n = 6), with an MIC90 of 16 mg/l for amoxycillin plus clavulanic acid was more resistant than either M. tuberculosis or M. bovis. Ticarcillin plus clavulanic acid with an MIC90 of 32 mg/l was less active against M. tuberculosis (n = 28) than amoxycillin plus clavulanic acid. The addition of clavulanic acid to amoxycillin greatly improves its in-vitro activity against M. tuberculosis and M. bovis.

Amoxicillin↗
PubMed1988

Utilization and metabolism of NAD by Haemophilus parainfluenzae.

The utilization of exogenous nicotinamide adenine dinucleotide (NAD) by Haemophilus parainfluenzae was studied in suspensions of whole cells using radiolabelled NAD, nicotinamide mononucleotide (NMN), and nicotinamide ribonucleoside (NR). The utilization of these compounds by H. parainfluenzae has the following characteristics. (1) NAD is not taken up intact, but rather is degraded to NMN or NR prior to internalization. (2) Uptake is carrier-mediated and energy-dependent with saturation kinetics. (3) There is specificity for the beta-configuration of the glycopyridine linkage. (4) An intact carboxamide groups is required on the pyridine ring. The intracellular metabolism of NAD was studied in crude cell extracts and in whole cells using carbonyl-14C-labelled NR, NMN, NAD, nicotinamide, and nicotinic acid as substrates in separate experiments. A synthetic pathway from NR through NMN to NAD that requires Mg2+ and ATP was demonstrated. Nicotinamide was found as an end-product of NAD degradation. Nicotinic acid mononucleotide and nicotinic acid adenine dinucleotide were not found as intermediates. The NAD synthetic pathway in H. parainfluenzae differs from the Preiss-Handler pathway and the pyridine nucleotide cycles described in other bacteria.

Glucose↗
PubMed1987

Comparative in vitro activities of ampicillin, BMY 28142, and imipenem against Mycobacterium avium complex.

The in vitro activity of ampicillin, BMY 28142, and imipenem was evaluated against 21 clinical isolates of Mycobacterium avium complex by both a broth and an agar dilution method. The MIC90 by broth dilution for ampicillin, BMY 28142, and imipenem was 16 micrograms/ml, 8 micrograms/ml, and greater than 32 micrograms/ml, respectively. The MIC90 by agar dilution for ampicillin and BMY 28142 was 16 micrograms/ml.

Ampicillin↗
PubMed1987

Comparison of four beta-lactamase inhibitors in combination with ampicillin against Mycobacterium tuberculosis.

The in-vitro activity of a beta-lactamase inhibitor (clavulanic acid, sulbactam, BL-P2013 or BL-P2090) in combination with ampicillin against 13 isolates of Mycobacterium tuberculosis was determined by broth dilution. The agents were tested in 1:1 molar ratio of ampicillin to beta-lactamase inhibitor. The beta-lactamase inhibitors alone did not inhibit growth at the highest concentration tested. The MIC90 for ampicillin alone was greater than 32 mg/l. Clavulanic acid plus ampicillin was the most active combination with an MIC90 of 11 microM (4 mg/l of ampicillin). The MIC90 of ampicillin in combination with sulbactam, BL-P2013 or BL-P2090 was 23 microM (8 mg/l of ampicillin). A 1:1 ratio of ampicillin to inhibitor was more active than was a 2:1 ratio. The addition of a beta-lactamase inhibitor to ampicillin greatly improves its in-vitro activity against M. tuberculosis.

Ampicillin↗
PubMed1986

Comparative in vitro activities of ciprofloxacin and other 4-quinolones against Mycobacterium tuberculosis and Mycobacterium intracellulare.

The in vitro activity of ciprofloxacin, ofloxacin, amifloxacin, and norfloxacin against 22 clinical isolates of Mycobacterium tuberculosis was evaluated by agar dilution. The MICs for 90% of the isolates of ciprofloxacin and ofloxacin were 0.5 and 1 microgram/ml, respectively. Amifloxacin and norfloxacin were less active. The MICs for 90% of the isolates of ciprofloxacin and ofloxacin against 20 clinical isolates of Mycobacterium intracellulare were determined by agar dilution to be 2 and 8 micrograms/ml, respectively.

Anti-Bacterial Agents↗
PubMed1985

Comparative in vitro activities of MDL 473, rifampin, and ansamycin against Mycobacterium intracellulare.

The susceptibilities of 20 clinical isolates of Mycobacterium intracellulare to rifampin, MDL 473, and ansamycin were determined by broth and agar dilution methods. Ansamycin was more active than MDL 473, which in turn was usually more active than rifampin by either method. The MICs for 90% of the strains tested by agar dilution were 1, 2, and 4 micrograms of ansamycin, MDL 473, and rifampin per ml, respectively.

Anti-Bacterial Agents↗
PubMed1983

In vitro susceptibility of Mycobacterium fortuitum to amoxicillin or cephalothin in combination with clavulanic acid.

The comparative in vitro activity of cefoxitin, cephalothin, amoxicillin, and clavulanic acid in combination with the latter two agents against 13 isolates of Mycobacterium fortuitum was evaluated by agar dilution susceptibility testing. Amoxicillin was more active than cephalothin but less active than cefoxitin against the strains tested. Clavulanic acid in combination with these beta-lactams usually improved the activity by one or two dilutions compared with the beta-lactams alone.

Amoxicillin↗
PubMed1983

In vitro activity of amoxicillin in combination with clavulanic acid against Mycobacterium tuberculosis.

The comparative in vitro activity of amoxicillin alone and in combination with clavulanic acid against 15 isolates of Mycobacterium tuberculosis was evaluated by broth dilution susceptibility testing. Amoxicillin inhibited 4 of 15 isolates at 8 micrograms/ml or less but was not bactericidal against any of the isolates at that concentration. Amoxicillin in combination with clavulanic acid was bactericidal for 14 of 15 isolates tested at an amoxicillin concentration of 4 micrograms/ml or less and a clavulanic acid concentration of 2 micrograms/ml or less.

Amoxicillin↗
PubMed1982

In vitro susceptibility of Mycobacterium fortuitum to N-formimidoyl thienamycin and several cephamycins.

The comparative in vitro activity of N-formimidoyl thienamycin, cefmetazole, cefoxitin, cefotetan (YM-09330), and moxalactam against 13 isolates of Mycobacterium fortuitum was evaluated by agar dilution susceptibility testing. N-Formimidoyl thienamycin inhibited 10 to 12 strains at 6.25 micrograms/ml, cefmetazole inhibited 12 of 13 strains at 12.5 micrograms/ml, cefoxitin inhibited 11 of 13 strains at 25 micrograms/ml, and cefotetan inhibited 11 of 13 strains at 50 micrograms/ml. Moxalactam was less active than the other compounds tested, inhibiting only 9 of 13 strains at 50 micrograms/ml.

Anti-Bacterial Agents↗