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Results for “Chloramphenicol Resistance”

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At least 19 recordsLinked to original sources
PubMed1981

Altered ribosomal RNA genes in mitochondria from mammalian cells with chloramphenicol resistance.

Chloramphenicol resistance in mammalian cells is cytoplasmically inherited. In yeast, a similar phenotype is caused by mutations in the mitochondrial DNA (mtDNA), and sequencing of carefully constructed strains has identified nucleotide monosubstitutions in the 3' region of the large (21S) rRNA gene which correlate with the antibiotic resistance. We have sequenced the corresponding section of mammalian mtDNA from chloramphenicol-resistant cell lines for comparison with the wild-type sequence. Differences between the sequences occur at positions similar to those altered in the yeast mutants, in a highly conserved region of the large (16S) rRNA gene.

Animals↗
PubMed1975

Comparison of trimethoprim-sulfamethoxazole and amoxicillin in therapy of chloramphenicol-resistant and chloramphenicol-sensitive typhoid fever.

The efficacy of orally administered trimethoprim-sulfamethoxazole was compared with that of oral amoxicillin in therapy of typhoid fever due to both epidemic chloramphenicol-resistant and endemic chloramphenicol-sensitive Salmonella typhi. Both drug regimens were effective and of comparable value in treatment of chloramphenicol-resistant infections, as measured by duration of fever (124 hr and 115 hr, respectively) and duration of bacteremia (1.0 and 0.4 days, respectively). Trimethoprim-sulfamethoxazole therapy of infections due to chloramphenicol-sensitive S. typhi resulted in more rapid lysis of fever than did amoxicillin therapy. Trimethoprim and sulfamethoxazole were not synergistic in vitro against the chloramphenicol-resistant strain of S. typhi, and the role of sulfamethoxazole in treatment of such infections appears to be minimal. Oral administration of trimethoprim-sulfamethoxazole is effective therapy of chloramphenicol-resistant, and probably of ampicillin-amoxicillin-resistant, typhoid fever.

Adolescent↗
PubMed1982

Rosanilins: indicator dyes for chloramphenicol-resistant enterobacteria containing chloramphenicol acetyltransferase.

Rosanilin dyes such as crystal violet and basic fuchsin have been used as indicator dyes in solid growth medium for chloramphenicol-resistant enterobacterial colonies containing the enterobacterial resistance enzyme chloramphenicol acetyltransferase (CAT). On certain media containing rosanilins, cells containing CAT formed darker colonies than cells not containing CAT. Contrast was affected by the types and concentrations of complex nutrients, sugars salts, and rosanilin dyes present. When crystal violet was used as the indicator dye, contrast could not be obtained for strains whose growth was partially inhibited by crystal violet. Contrast could not be obtained between yeast colonies with and without the enterobacterial resistance enzyme, between Bacillus subtilis colonies with and without the staphylococcal resistance enzyme, or between enterobacterial colonies with and without the staphylococcal resistance enzyme. The darker coloration of enterobacterial colonies with the enterobacterial enzyme was due to the binding of dye to enzyme. Rosanilin dues have been used to score resistance phenotypes by colony color, to detect chloramphenicol-sensitive sectors in chloramphenicol-resistant colonies, and to screen for occasional chloramphenicol-sensitive cells in a resistant population during cloning by insertional inactivation of the chloramphenicol resistance gene.

Acetyltransferases↗
PubMed2005

The chloramphenicol resistance gene cmlA is disseminated on transferable plasmids that confer multiple-drug resistance in swine Escherichia coli.

A recent study of beta-hemolytic Escherichia coli isolated from diarrheic swine found that 53% were resistant to chloramphenicol, a drug that has been prohibited from use in food animals in the US since the mid-1980s. To identify the factors governing the persistence of chloramphenicol resistance in the absence of specific selection pressure, the location of the chloramphenicol resistance gene cmlA and its linkage to other resistance determinants were investigated. Southern blot analysis of plasmid DNA from 46 swine E. coli isolates indicated that cmlA was present on large plasmids greater than 100 kbp. Fifty-two percent of the isolates were able to transfer chloramphenicol resistance to an E. coli recipient at conjugation frequencies ranging from 10(-3) to 10(-8) per recipient. Antimicrobial susceptibility tests on transconjugant strains demonstrated that resistance to sulfamethoxazole, tetracycline, and kanamycin frequently transferred along with chloramphenicol resistance. The transconjugant strains possessed at least two distinct class 1 integrons that linked cmlA to both aminoglycoside resistance genes aadA1 and aadA2 and either to sul1 or to sul3 sulphonamide resistance genes. These results suggest that in the absence of specific chloramphenicol selection pressure, the cmlA gene is maintained by virtue of gene linkage to genes encoding resistance to antimicrobials that are currently approved for use in food animals.

Animals↗
PubMed1978

Detection of conjugative R plasmids conferring chloramphenicol resistance in Escherichia coli isolated from domestic and feral pigeons and crows.

A total of 87 domestic pigeons of 2 lots and 184 feral pigeons of 15 lots were examined from 1975 to 1977 for the presence of drug-resistant (especially chloramphenicol resistant) Escherichia coli. 20 (23.0%) of the domestic pigeons of the 2 lots, and 39 (21.2%) of the feral pigeons of 5 lots (33,3%) showed resistant E. coli. Usage of selective media containing chloramphenicol, streptomycin or tetracycline resulted in the increase in isolation frequency of resistant E. coli excepting one lot of domestic pigeons in which isolation of chloramphenicol resistant E. coli was very frequent without selection by the drug. Among a total of 106 resistant E. coli isolates from pigeons, 64 (60.4%) were multiply resistant and 58 of the 64 isolates were resistant to chloramphenicol. 58 (90.6%) of the multiply resistant E. coli carried conjugative R plasmids, including 13 thermosensitive R plasmids. 8 (19.0%) of 42 singly resistant E. coli isolates had conjugative R plasmids. 10 crows of 2 lots were examined similarly. Half of them had resistant E. coli. 15 (78.9%) of a total of 19 resistant E. coli isolates were multiply resistant. Of the 15 multiply resistant E. coli isolates, 5, from 2 Japanese jungle crows, were resistant to chloramphenicol. 11 (73.3%) of the 15 multiply resistant isolates carried conjugative R plasmids, including one thermosensitive R plasmid. Difference of drug resistance status between Salmonella and E. coli isolated from pigeons was discussed.

Animals↗
PubMed1975

Studies on the development of chloramphenicol resistance in Salmonella typhimurium.

Chloramphenicol therapy of acute and chronic Salmonella typhimurium infection in mice did not lead to the development of chloramphenicol resistant mutants of this organism. However, chloramphenicol resistant organisms were readily produced in vitro. Transfer of chloramphenicol resistance from a donor strain of Escherichia coli X12 to a suitable recipient strain of S typhimurium 5235 occurred readily in the intestine of 15 out of 20 conventional mice, following oral administration of large doses of these strains supplemented by chloramphenicol therapy. When a similar system was used in untreated animals, only a small number of chloramphenicol resistant S typhimurium were isolated from three out of 18 mice. The virulence of chloramphenicol resistant S typhimurium produced in vitro and in vivo was similar to that of the sensitive parent strain.

Animals↗
PubMed1985

A permeability barrier as a mechanism of chloramphenicol resistance in Haemophilus influenzae.

Chloramphenicol resistance in Haemophilus influenzae occurs most frequently via plasmid-mediated chloramphenicol acetyltransferase production. We studied four strains with high-level chloramphenicol resistance (MIC greater than 20 micrograms/ml) which did not have detectable chloramphenicol acetyltransferase activity. The chloramphenicol resistance determinant was transformed into a chloramphenicol-susceptible laboratory H. influenzae strain from each of the four wild-type strains, enabling isogenic comparisons. By thin-layer chromatography and a bioassay, there was no evidence of non-chloramphenicol acetyltransferase modification of chloramphenicol. In vitro protein synthesis in the presence of chloramphenicol was equivalently inhibited in the chloramphenicol-resistant transformants and in the susceptible recipient. Chloramphenicol uptake by these strains during logarithmic growth was compared by high-pressure liquid chromatographic quantitation; at chloramphenicol concentrations of 5, 10, and 20 micrograms/ml the four transformants showed a decreased rate of uptake of chloramphenicol compared with the isogenic chloramphenicol-susceptible recipient. Sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis of outer membrane proteins revealed a markedly diminished 40-kilodalton protein in the resistant transformants. We propose that the mechanism of chloramphenicol resistance in these strains is a relative permeability barrier due to the loss of an outer membrane protein.

Acetyltransferases↗
PubMed1991

The problem of emerging chloramphenicol resistance in typhoid fever--a preliminary report.

Drug sensitivity of Salmonella typhi isolated from 25 blood culture positive cases of typhoid fever who presented between May and July 1990 was tested to determine their in vitro susceptibility to various antimicrobials. Twenty-one of them (84%) showed resistance to chloramphenicol and 24 (96%) to cotrimoxazole. All the 25 cases were sensitive to norfloxacin, gentamicin and cephalexin. Sixteen of 21 chloramphenicol resistant typhoid cases in whom chloramphenicol was initially started failed to respond to this drug even after 5 to 7 days, thereby indicating that in vivo response matched with the in vitro sensitivity. Clinical response to norfloxacin, whether given initially or following chloramphenicol failure, was prompt and satisfactory. Norfloxacin thus appears to be a good choice in such cases.

Chloramphenicol↗
PubMed2004

Chloramphenicol resistance in vancomycin-resistant enterococcal bacteremia: impact of prior fluoroquinolone use?

OBJECTIVE: The prevalence of vancomycin-resistant enterococci (VRE) has increased markedly during the past decade. Few data exist regarding the epidemiology of resistance of VRE to chloramphenicol, one of the few therapeutic options. DESIGN: Survey and case-control study. SETTING: A 725-bed, tertiary-care academic medical center and a 344-bed urban community hospital. PATIENTS: Hospitalized patients with blood cultures demonstrating VRE. METHODS: We examined the trends in the prevalence of chloramphenicol resistance in VRE blood isolates at our institution from 1991 through 2002 and conducted a case-control study to identify risk factors for chloramphenicol resistance among these isolates. RESULTS: From 1991 through 2002, the annual prevalence of chloramphenicol-resistant VRE increased from 0% to 12% (P < .001, chi-square test for trend). Twenty-two case-patients with chloramphenicol-resistant VRE bloodstream isolates were compared with 79 randomly selected control-patients with chloramphenicol-susceptible VRE. Independent risk factors for chloramphenicol-resistant VRE were prior chloramphenicol use (odds ratio [OR], 10.9; 95% confidence interval [CI95], 1.72-68.91; P = .01) and prior fluoroquinolone use (OR, 4.74; CI95, 1.15-19.42; P = .03). Chloramphenicol-resistant VRE isolates were more likely to be susceptible to beta-lactams and resistant to tetracycline than were chloramphenicol-susceptible VRE isolates. CONCLUSIONS: Significant increases in the prevalence of chloramphenicol-resistant VRE may limit the future utility of chloramphenicol in the treatment of VRE infections, and close monitoring of susceptibility trends should continue. The association between fluoroquinolone use and chloramphenicol-resistant VRE, reflecting possible co-selection of resistance, suggests that recent dramatic increases in fluoroquinolone use may have broader implications than previously recognized.

Bacteremia↗
PubMed1993

Chloramphenicol resistant typhoid fever.

We report a patient with typhoid fever caused by a strain of Salmonella typhi which was resistant to chloramphenicol. This is the first documentation of chloramphenicol resistant Salmonella typhi in Sri Lanka.

Adult↗