Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Salmonella typhimurium S24 was isolated in September 1986 at Kaohsiung Medical College Hospital, Kaohsiung, Taiwan, from a patient suffering from gastroenteritis during an outbreak of salmonellosis. Two conjugative R-plasmids have been isolated from Escherichia coli K-12 14R525, which was mated with S. typhimurium S24. The two R-plasmids found in S. typhimurium S24 belong to two different incompatibility (Inc) groups: the 130-kilobase IncFI plasmid pST1 and the 56-kb IncN plasmid pST2. These two R-plasmids of pST1 and pST2 together mediate resistance to multiple antibiotics in S. typhimurium S24. By DNA probes hybridization, plasmid pST1 was shown to carry an enteric type II chloramphenicol acetyltransferase (CAT) gene, a class C tetracycline resistance (TetR) gene and a type III dihydrofolate reductase (DHFR) gene, all of which confer resistance to chloramphenicol, tetracycline, and trimethoprim respectively. A Richmond's type III beta-lactamase gene was located on each plasmid of pST1 and pST2. beta-lactamases specified by both plasmids pST1 and pST2 conferred high level resistance to amoxicillin, carbenicillin, piperacillin, sulbenicillin, ticarcillin in addition to ampicillin. A novel aminoglycoside 6'-N-acetyltransferase [AAC(6')] was demonstrated on plasmid pST2. This AAC(6') enzyme modified kanamycin, amikacin, dibekacin, tobramycin, gentamicin, netilmicin, sisomicin, butirosin and ribostamycin.
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PMID:Molecular characterization of R-plasmids pST1 and pST2 from Salmonella typhimurium S24. 143 39

Anaerobic bacteria currently demonstrate increased resistance to antimicrobial agents, primarily by the production of beta-lactamase. A number of species of Bacteroides, most notably those in the Bacteroides fragilis group, produce these enzymes. A few species of Fusobacterium and Clostridium produce beta-lactamase as well. Fortunately, this mechanism of resistance is readily overcome by administering beta-lactamase inhibitors coupled with a beta-lactam antibiotic that would otherwise be inactivated. Other types of resistance encountered in anaerobic bacteria include inactivating enzymes such as chloramphenicol acetyltransferase, plasmid-mediated transferable multiple-drug resistance, changes in porin molecules in the outer membrane of the bacterial cell, decreased uptake of drug by other mechanisms, changes in the target organs such as penicillin-binding proteins, and decreased reduction of the antibiotic to an active intermediate product. In many institutions, certain drugs such as cefoxitin, clindamycin, and piperacillin, which were previously active against almost all strains of B. fragilis, are now effective against only 70 to 85% of this group of anaerobes. Drugs with essentially 100% activity against most anaerobic bacteria include chloramphenicol, imipenem, metronidazole, and the combinations of a beta-lactam antibiotic plus a beta-lactamase inhibitor such as ampicillin plus sulbactam and amoxicillin or ticarcillin combined with sodium clavulanate. This paper also discusses the indications for antimicrobial susceptibility testing of anaerobes as well as problems encountered with testing techniques that are currently being used.
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PMID:Mechanisms of resistance in anaerobes and new developments in testing. 268 14

Three clinical isolates of Haemophilus ducreyi, representing at least two subtypes, were shown to be resistant to streptomycin and kanamycin. They also produced a beta-lactamase and chloramphenicol acetyltransferase and were resistant to tetracycline. In the three strains the resistance to both aminoglycoside antibiotics was encoded by a plasmid of ca. 4.7 kilobases which apparently did not carry ampicillin, chloramphenicol, or tetracycline resistance genes, as determined after transfer to Escherichia coli by transformation. Resistance to streptomycin and kanamycin was due to the presence of two aminoglycoside phosphotransferases (APH). The enzyme modifying kanamycin was a 3',5"-APH of type I [APH(3',5")-I], as inferred from its substrate profile and immunological cross-reactivity with the APH(3',5")-I encoded by the transposable element Tn903. However, the APH(3',5")-I gene in H. ducreyi did not appear to be carried by Tn903.
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PMID:Plasmid-mediated aminoglycoside phosphotransferases in Haemophilus ducreyi. 301 Aug 43

The uptake and expression by plastids isolated from dark-grown cucumber cotyledons (etioplasts) of two pUC derivatives, pCS75 and pUC9-CM, respectively carrying genes for the large small subunits of ribulose bisphosphate carboxylase/oxygenase of Anacystis nidulans or chloramphenicol acetyltransferase, is reported. Untreated etioplasts take up only 3% as much DNA as that taken up by EDTA-washed etioplasts after 2 hr of incubation with nick-translated [32P]-pCS75. The presence or absence of light does not affect DNA uptake, binding, or breakdown by etioplasts. Calcium or magnesium ions inhibit DNA uptake by 86% but enhance binding (23-200%) and breakdown (163-235%) of donor DNA by EDTA-treated etioplasts. Uncouplers that abolish membrane potential (delta psi), transmembrane proton gradient (delta pH), or both do not affect DNA uptake, binding, or breakdown by etioplast. However, both DNA uptake and binding are severely inhibited by ATP. Presumably this results from the hydrolysis of ATP, because the poorly hydrolyzable analog adenyl-5'-yl imidodiphosphate does not inhibit the uptake or binding of DNA by etioplasts. beta-Lactamase specified by the ampicillin resistance gene of pCS75 can be detected only in EDTA-treated etioplasts that have been incubated with the plasmid pCS75. After the incubation of EDTA-treated etioplasts with pCS75, immunoprecipitation using antiserum to the small subunit of ribulose bisphosphate carboxylase/oxygenase from A. nidulans reveals the synthesis of small subunits; these are smaller by 2 kDa than the cucumber small subunit encoded by the nuclear genome. Treatment of etioplasts with 10 mM EDTA shows a 10-min duration to be optimal for the expression of chloramphenicol acetyltransferase encoded by pUC9-CM. A progressive increase in the expression of this enzyme is observed with an increase in the concentration of pUC9-CM in the DNA uptake medium. The plasmid-dependent incorporation of [35S]methionine by EDTA-treated organelles declines markedly during cotyledon greening in vivo.
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PMID:Uptake and expression of bacterial and cyanobacterial genes by isolated cucumber etioplasts. 311 48

A total of 2,811 clinical isolates of Haemophilus influenzae were obtained during 1986 from 30 medical centers and one nationwide private independent laboratory in the United States. Among these, 757 (26.9%) were type b strains. The overall rate of beta-lactamase-mediated ampicillin resistance was 20.0%. Type b strains were approximately twice as likely as non-type b strains to produce beta-lactamase (31.7 versus 15.6%). The MICs of 12 antimicrobial agents were determined for all isolates. Ampicillin resistance among strains that lacked beta-lactamase activity was extremely uncommon (0.1%). Percentages of study isolates susceptible to cefamandole, cefaclor, cephalothin, and cephalexin were 98.7, 94.5, 87.3, and 43.3%, respectively. For 14 strains (0.5% of the total), chloramphenicol MICs were greater than or equal to 8.0 micrograms, and thus the strains were considered resistant. All of these resistant strains produced chloramphenicol acetyltransferase. In addition, all 14 strains were resistant to tetracycline; 11 produced beta-lactamase. The percentage of isolates susceptible to tetracycline was 97.7%. In contrast, erythromycin and sulfisoxazole were relatively inactive. The combination of erythromycin-sulfisoxazole (1/64) was more active than erythromycin alone but essentially equivalent in activity to sulfisoxazole alone. Finally, small numbers of clinical isolates of H. influenzae were resistant to trimethoprim-sulfamethoxazole and rifampin.
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PMID:National collaborative study of the prevalence of antimicrobial resistance among clinical isolates of Haemophilus influenzae. 325 21

A 4-month-old infant with congenital heart disease and sepsis and arthritis, and subsequently meningitis, caused by an antibiotic-resistant strain of Haemophilus influenzae type b, failed to respond to sequential therapy with ampicillin and trimethoprim/sulfamethoxazole. Following treatment with ceftizoxime, the infant was well for 42 days, until he returned to the hospital and died. A total of 10 Haemophilus influenzae type b isolates, all outer membrane protein subtype 51, was isolated from the pretreatment blood and synovium, cerebrospinal fluid and subdural fluids, and the petrous pyramids at autopsy. Pretreatment isolates had no detectable plasmid DNA, chloramphenicol acetyltransferase or beta-lactamase; the minimal inhibitory concentration for ampicillin (AM) and chloramphenicol (CM) was 0.2 and 0.8 microgram/ml, respectively. However, all cerebrospinal fluid isolates had a 42-44 mD plasmid and produced chloramphenicol acetyltransferase and beta-lactamase; the minimal inhibitory concentration of these isolates to AM and CM were 12.5 and 25 micrograms/ml, respectively, and were also resistant to tetracycline and sulfonamide. Resistance to AM and CM was cotransferred by filter-mating conjugation at a frequency of one to two transconjugants per 10(5) to an Rd haemophilus recipient. Posttreatment isolates from the petrous pyramids also were resistant to AM and CM and produced chloramphenicol acetyltransferase and beta-lactamase activity, but had no plasmid DNA. These findings and data from genetic studies suggested that plasmid-bearing antibiotic-resistant Haemophilus influenzae type b was selected from a heterogenous population, and that the AM/CM resistance transposons were incorporated into the bacterial chromosome.
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PMID:Ampicillin-chloramphenicol-resistant Haemophilus influenzae: plasmid-mediated resistance in bacterial meningitis. 350 Apr 49

The prevalence of antibiotic resistance in Haemophilus influenzae is increasing. The encapsulated strains of group b are the strains that are most important in the pathogenesis of severe systemic infections, and it is in this group that the incidence of resistance is highest. Strains simultaneously resistant to ampicillin, chloramphenicol, and tetracycline are rare but have been isolated in several parts of the world. Transferable antibiotic resistance is well documented, and both small (3.6 megadaltons) and large (38-42 megadaltons) plasmids mediating beta-lactamase and chloramphenicol acetyltransferase production and tetracycline resistance have been detected in H. influenzae. The possibilities for treatment of infections due to such organisms include the use of the newer cephalosporins, of a combination of a beta-lactamase inhibitor and ampicillin, and of alternate agents such as minocycline and trimethoprim. Sporadic strains resistant to these agents have also been reported.
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PMID:Antibiotic resistance in Haemophilus influenzae: epidemiology, mechanisms, and therapeutic possibilities. 354 Nov 36

We evaluated the in vitro antimicrobial activity of Sch 24893, Sch 25298, and Sch 25393, three novel analogs of chloramphenicol and thiamphenicol. All of the analogs had minimal inhibitory concentrations of less than or equal to 10 micrograms/ml for 18 chloramphenicol-thiamphenicol-resistant strains of Shigella dysenteriae and 21 strains of resistant Salmonella typhi. The analogs were also more active than were chloramphenicol and thiamphenicol against chloramphenicol-resistant enteric bacteria, including six strains of Escherichia coli, seven strains of Klebsiella pneumoniae, and two strains of Enterobacter cloacae. Fifty-three strains of ampicillin-resistant Haemophilus influenzae were uniformly susceptible to chloramphenicol, thiamphenicol, and the three analogs. Sch 25298 was the most active compound tested (minimal inhibitory concentration, 0.5 microgram/ml for all strains). Four of seven chloramphenicol-thiamphenicol-resistant Haemophilus strains were susceptible to the fluorinated analogs. Of the three Haemophilus strains which were resistant to chloramphenicol, thiamphenicol, and the analogs, two contained less than 10% of the chloramphenicol acetyltransferase activity of the strains which were resistant to only chloramphenicol and thiamphenicol. We conclude that fluorinated analogs of chloramphenicol and thiamphenicol have considerable in vitro activity against a broad spectrum of chloramphenicol-thiamphenicol-resistant, gram-negative bacteria.
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PMID:In vitro antibacterial activity of fluorinated analogs of chloramphenicol and thiamphenicol. 695 62

We examined nine chloramphenicol-resistant (minimal inhibitory concentration, greater than or equal to 15 micrograms/ml) Haemophilus influenzae strains isolated in various parts of the world to characterize the genetic and biochemical bases of the resistance; four were type b. All nine contained conjugative plasmids, ranging in molecular weight from 34 x 10(6) to 46 x 10(6), which encoded for resistance to chloramphenicol and tetracycline or chloramphenicol, tetracycline, and ampicillin. Deoxyribonucleic acid homology studies showed that these plasmids were closely related to a previously described ampicillin-resistant plasmid, RSF007, and to each other. All nine isolates and their chloramphenicol-resistant transconjugants produced chloramphenicol acetyltransferase. We conclude that chloramphenicol resistance in these strains of H. influenzae is via plasmid-mediated production of chloramphenicol acetyltransferase.
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PMID:Characterization of chloramphenicol-resistant Haemophilus influenzae. 696 77

The minimal inhibitory concentration (MIC) of chloramphenicol for a clinical isolate of Haemophilus ducreyi, strain CEB-10, was 16 micrograms/ml. This strain was also resistant to tetracycline (MIC = 64 micrograms/ml) and ampicillin. The presence of a chloramphenicol acetyltransferase (CAT) activity was demonstrated.
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PMID:Detection of chloramphenicol acetyltransferase (CAT) activity in a strain of Haemophilus ducreyi. 698 23


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