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PubMedDate not supplied

Induced multidrug-resistance in murine sarcoma 180 cells grown in vitro and in vivo and associated changes in expression of multidrug-resistance DNA-sequences and membrane glycoproteins.

The aim of this investigation was to analyze the resistance to doxorubicin and daunorubicin of murine sarcoma 180 cells grown in vitro (monolayer) and in vivo (ascites form). The colchicine-resistant CHO cells were used as controls. A multidrug-resistant phenotype was found in all investigated cell lines. Multidrug resistant cells grown in tissue culture or as ascites tumor cells needed more time to accumulate rhodamine 123 than their sensitive parental cells. In order to evaluate whether the resistant cells show alterations in the plasma membranes, different methods were applied (immunocytochemistry, immunofluorescence, immunoblotting) using the monoclonal antibodies 265/F4 and C 219. These methods all revealed an increased expression of the glycoprotein Mr 170 kd in the multidrug-resistant cell lines. To determine whether multidrug DNA sequences were expressed in the resistant cell lines, slot blots and Northern blots with RNA of sensitive and resistant cells were performed using the clones pDR 7.8 and pcDR 1.5. Elevated RNA levels were detected in all resistant cell lines.

Animals↗
PubMed1985

Heat-resistant mutants of B-16 melanoma cells. I. Stepwise heating in vitro induces progressive increase in resistance to heat.

Cloned lines from 4 different families of B-16 melanoma cells were heated repeatedly in tissue culture at 45 degrees C with step-up time intervals. These lines included the partially heat-resistant lines previously selected at 43 degrees C(HR 43 degrees) from wheat-germ-agglutinin-resistant mutant (WGAR, HR43 degrees), concanavalin-resistant mutant (conR-HR 43 degrees), ricin-resistant mutant (ricinR, HR 43 degrees), and parental B-16 (B-16, HR 43 degrees) cells. The heating cycles were repeated 7 to 11 times at 45 degrees C increasing from 45 min to 150 min with 3 weeks of culturing at 37 degrees C between cycles. Heat resistance in most cases increased progressively with each heating step. An extensive library of mutants was thus generated, varying in the degree of heat resistance and the apparent stability. HR variants from the WGAR family appeared to be the most resistant and the most stable. The heat-resistant phenotype was expressed not only by increased survival after a normally lethal heat dose, but also by protection against heat-mediated suppression of proteins and DNA syntheses. Protein synthesis in the heat-resistant cells was not only less suppressed by heat shock, but also recovered more rapidly after removal of shock. Clinical implications of these results and the potential usefulness of the mutant lines for genetic studies are discussed.

Adaptation, Physiological↗
PubMed1983

Differential tumor immunogenicity of DBA/2 mouse lymphoma L1210 and its sublines. III. Control of host resistance to drug-resistant L1210 sublines by H-2-linked and non-H-2-linked genes.

The effects of the host's genetic composition on the host's resistance to the DBA/2 L1210 lymphoma and three drug-resistant L1210 sublines (which show an increased expression of tumor-associated antigens) were investigated. Histocompatible F1 mice between DBA/2 and other mouse strains were given injections ip of graded numbers of these tumor cells, and a marked difference in the resistance of the host to tumor growth was demonstrated. The resistant hybrid mice showed markedly higher resistance to the L1210 sublines than to the L1210 parent lymphoma cells. Experiments with F1 mice between DBA/2 (H-2d) and certain congeneic intra-H-2 recombinant strains showed that the H-2b/d heterozygosity at the H-2K+l-A regions and additional non-H-2 genetic factor(s) confer the resistance to the F1 mice. The resistance was abolished by treating host animals with injections of silica, an antimacrophage agent, or rabbit anti-mouse thymocyte serum. These results suggest that the resistance is immunologic and that the genetically controlled host resistance may be directed to surface changes related to the increased expression of tumor-associated antigens.

Animals↗
PubMed1984

Establishment of human KB cells resistant to 1-beta-D-arabinofuranosylcytosine, and mechanisms of cellular resistance in isolated clones.

A subline of human KB cells that was resistant to 1-beta-D-arabinofuranosylcytosine (ara-C) was established by continuous exposure of the cells to increasing concentrations of ara-C. Thirteen resistant clones were isolated from the resistant subline (KB/ara-C). KB/ara-C showed 1,300-fold higher resistance than the parent KB cells to ara-C; the most resistant clones, clones 7 and 10, showed 1,330-fold higher resistance. In the absence of ara-C, the resistance of the parent KB/ara-C cells was stable for at least 14 weeks, whereas that of clone 7 was stable for 10 weeks, but was slightly less after 14 weeks. The ara-C kinase and ara-C deaminase activities of the 13 clones and the cellular uptake of ara-C by several clones were measured. In general the clones showed decreased deoxycytidine kinase activity and decreased cellular uptake of ara-C. Most clones had higher cytidine deaminase activity than KB cells, but some had activity similar to that of the KB cells. A clear inverse relationship was found between the ara-C sensitivity of the clones and their kinase activity, but not their deaminase activity or their ara-C uptake. These results clearly demonstrate that a major mechanism of ara-C resistance of these human KB cells was a decrease in the activity of the ara-C activating enzyme deoxycytidine kinase. The parent KB/ara-C cells showed no clear cross-resistance to various antitumor agents other than an ara-C derivative, including metabolic inhibitors, alkylating agents, DNA binders and mitotic spindle poisons.

Antineoplastic Agents↗
PubMed1983

Development of resistance to glucocorticoid hormones during rat thymus cell differentiation: proteins associated with emergence of the resistant state.

Two-dimensional gel electrophoresis was used to detect [35S]methionine-labeled newly synthesized proteins from both glucocorticoid-sensitive and -resistant thymus cells. Normal thymic lymphocytes were taken for the sensitive population; the resistant population was composed of medullary thymocytes obtained from rats treated with dexamethasone (10 mg per kg body weight per day) for 3 days. When the proteins from glucocorticoid-sensitive cells are compared to those from resistant cells, the majority of the congruent to 1000 proteins were similar; however, 18 proteins were different. There were 13 proteins that increase in the resistant state and 5 that decrease. One major change is the appearance of a new protein with a molecular weight of about 36,000 in resistant rat thymocytes. This protein is in the same position on the gels as is a protein found in corticosteroid-resistant P1798 mouse lymphosarcoma cells but not in the corticosteroid-sensitive cells. Control experiments indicate that the protein differences are neither components of fibrous tissue associated with the cells nor components of blood. Changes in the synthesis of a common set of proteins that are characteristic of the hormone-resistant state suggest that the presence of one or more of these proteins may confer resistance. The appearance of a single protein in two distinctly different cell types suggests it as the most likely candidate. This coincidence further suggests that tumor cells become resistant by selection of those cells that can express the same gene product as do those normal cells as they undergo immunological commitment.

Animals↗
PubMed1982

[Amplification of portions of the genome in mammalian somatic cells resistant to colchicine. I. Chromosome 4 trisomy in the development of gene amplification and colchicine resistance in Djungarian hamster cells].

10 independent clones of Djungarian hamster DM-15 and DMCAP cells 16-22-fold resistant to colchicine were obtained. The drug resistance was unstable. During cultivation in a colchicine free medium, 1-2% cells per population doubling lost resistance to selective dosage of the drug (0,1 microgram/ml). The loss of colchicine resistance was stepwise: the cells lost resistance to some concentrations of the drug but retained resistance to the lower colchicine dosages toxic for the wild-type cells. The analysis of chromosomes stained by the trypsin G-banding technique showed the specific karyotypic alteration in all the cells of 10 clones, i.e. complete or partial trisomy of chromosome 4. In addition, in some cells of 7 clones small chromatin bodies (SCB) and chromosomes bearing long homogeneously staining regions (HSRs) were found. The loss of colchicine resistance was accompanied by the disappearance of cells containing SCB and HSRs and the decrease in the number of cells with trisomy 4. However, the direct correlation between the loss of drug resistance and that of additional material of chromosome 4 was not observed. Probably, the resistance to colchicine is connected in these clones with gene amplification, and trisomy 4 is involved in the development of gene amplification.

Animals↗
PubMed1994

Multidrug resistance-associated protein gene overexpression and reduced drug sensitivity of topoisomerase II in a human breast carcinoma MCF7 cell line selected for etoposide resistance.

A human breast cancer cell line (MCF7/WT) was selected for resistance to etoposide (VP-16) by stepwise exposure to 2-fold increasing concentrations of this agent. The resulting cell line (MCF7/VP) was 28-, 21-, and 9-fold resistant to VP-16, VM-26, and doxorubicin, respectively. MCF7/VP cells also exhibited low-level cross-resistance to 4'-(9-acridinylamino)-methanesulfon-m-anisidide, mitoxantrone, and vincristine and no cross-resistance to genistein and camptothecin. Furthermore, these cells were collaterally sensitive to the alkylating agents melphalan and chlorambucil. DNA topoisomerase II levels were similar in both wild-type MCF7/WT and drug-resistant MCF7/VP cells. In contrast, topoisomerase II from MCF7/VP cells appeared to be 7-fold less sensitive to drug-induced cleavable complex formation in whole cells and 3-fold less sensitive in nuclear extracts than topoisomerase II from MCF7/WT cells. Although this suggested that the resistant cells may contain a qualitatively altered topoisomerase II, no mutations were detected in either the ATP-binding nor the putative breakage/resealing regions of either DNA topoisomerase II alpha or II beta. In addition, the steady-state intracellular VP-16 concentration was reduced by 2-fold in the resistant cells, in the absence of detectable mdr1/P-gp expression and without any change in drug efflux. In contrast, expression of the gene encoding the MRP was increased at least 10-fold in resistant MCF7/VP cells as compared to sensitive MCF7/WT cells. These results suggest that resistance to epipodophyllotoxins in MCF7/VP cells is multifactorial, involving a reduction in intracellular drug concentration, possibly as a consequence of MRP overexpression, and an altered DNA topoisomerase II drug sensitivity.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Cross-resistance to cisplatin in cells resistant to photofrin-mediated photodynamic therapy.

This study shows that a Photofrin-induced photodynamic therapy-resistant variant (RIF-8A) of a radiation-induced fibrosarcoma-1 cell line (RIF-1) is cross-resistant to cis-diamminedichloroplatinum(II) (cisplatin). This is the first study to show cross-resistance to cisplatin in photodynamic therapy-resistant variants in vitro. Resistance does not appear to be the result of elevated glutathione levels since neither the resistant variant (RIF-8A) nor the parental line (RIF-1) varied in total glutathione levels. However, cisplatin-DNA adduct levels differed significantly between the two cell types. Immediately following a 1-h exposure to cisplatin (50 microM), RIF-1 cells contained 44.6 +/- 2.0 (SEM) pg platinum/micrograms DNA while RIF-8A cells contained 24.8 +/- 6.3 pg platinum/micrograms DNA. In addition, the resistant variant had decreased plasma and mitochondrial membrane potentials. The plasma and mitochondrial membranes of the resistant variant accumulated 3- and 3.6-fold less rhodamine 123, respectively. The difference in rhodamine 123 accumulation could not be attributed to elevated P-glycoprotein expression because both the parental line and the variant contained similar amounts of P-glycoprotein. In conclusion, alterations in the plasma and/or mitochondrial membrane potentials may provide cells with a survival advantage when challenged with either photodynamic therapy or cisplatin in vitro. This appears to be a novel mechanism of resistance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

[Studies on the problems of resistance to antituberculous drugs. II--1. Clinically applicable criteria of drug-resistance to rifampicin].

Preliminary studies showed that some strains of tubercle bacilli were inhibited even by 2 micrograms/ml of rifampicin (RFP), but 10 micrograms/ml or higher concentrations were needed for the inhibition of all strains. Of 5,100 patients with pulmonary tuberculosis who were admitted to our hospital during 12 years since January 1970 through 1981, 1,344 patients had no previous antituberculous drug therapy. All of the strains of Mycobacterium tuberculosis isolated from such 1,344 patients showed no or less than 10% growth of control on 10 micrograms-RFP medium by indirect susceptibility tests. But, I defined the clinically applicable criteria of resistance to RFP as "more than 1% growth of control on 10 micrograms-RFP medium" because of following reasons: 1) the growth more than 1% and less than 10% of control on 10 micrograms-RFP medium could be reasonably explained as the results of some technical failures, 2) the results of follow-up observations of respective cases, 3) our previous studies on the distribution of RFP-susceptibility of natural resistant strains. Among total 5,100 cases, 605 cases had been treated with antituberculous drugs previously but failed to achieve negative conversion of the bacilli, and restarted the treatment with regimen including RFP (retreatment group), and the remains had no previous treatment (initial treatment group). The negative conversion rates within three months of treatment were almost same (more than 95%) in both groups, but the rates of RFP-resistance were 5.6% for the initial treatment group and 92.8% for the retreatment group. Among 605 retreated cases 129 were susceptible to RFP at the start of the treatment but became resistant to RFP, of which 11 were resistant to 10 micrograms/ml and 118 to 50 micrograms/ml RFP. Two of the 11 10 micrograms-resistant cases remained to be 10 micrograms-resistant until their death (8 and 15 months after the start of the therapy, respectively) though their critical proportions showed some fluctuations. Remaining 9 cases later became resistant to 50 micrograms/ml RFP. By the 50 micrograms-resistant cases with lower critical proportion, the increase of critical proportion was rarely observed and did not reach even 50%. "Fall-and-rise" phenomena were observed rather frequently during the course of treatment with regimens including RFP. The decrease of the number of bacilli in sputa, sometimes to culture-negativity, at the initial phase of the treatment may be an evidence of killing of susceptible bacilli. If bacilli reappeared or increased their number, it is a critical time to reassess the treatment schedule.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

Yeast topoisomerase II mutants resistant to anti-topoisomerase agents: identification and characterization of new yeast topoisomerase II mutants selected for resistance to etoposide.

We describe a system that allows us to easily isolate and characterize mutants in yeast topoisomerase II that are resistant to antitumor agents that target this enzyme. The system uses yeast strains that are sensitive to those agents and that carry temperature-sensitive top2 mutations. The temperature-sensitive mutation allows the isolation of recessive drug-resistant mutations. The mutagenized TOP2 gene we have used is under the control of the yeast DED1 promoter; this overexpression of TOP2 is designed to avoid isolating mutants that are drug resistant solely because the mutated topoisomerase II has low enzymatic activity. We describe three mutants that we isolated using this system. Two of the three mutants show resistance to etoposide and amsacrine, while the third mutant is partially resistant to etoposide and fluoroquinolones but not to amsacrine. DNA sequence changes have been identified in all of these mutant TOP2 genes. The mutant with partial resistance to etoposide and fluoroquinolones has an amino acid change at position 738 of TOP2, which is three amino acids from the site homologous to Ser83 of E. coli gyrA, an amino acid which had previously been shown to be an important target for resistance to quinolones in bacteria. One of the alleles that confers resistance to both etoposide and amsacrine, top2-103, has changes in amino acid 824 and amino acid 1186 of TOP2. Reconstruction of the mutations by oligonucleotide-directed mutagenesis demonstrates that the change at amino acid 824 is responsible for the drug resistance of this allele.

Amino Acid Sequence↗
PubMed1996

[Actinomycin D resistance of gramicidin-resistant strains of Staphylococcus].

Factors defining actinomycin D resistance in Staphylococcus aureus resistant to gramicidin S were investigated. The results of the thin layer chromatography, high-voltage electrophoresis and bioautography showed that the resistant cells did not inactivate actinomycin D by the hydrolysis of the lactone bond in the antibiotic molecule. The estimation of the cell ability to bind actinomycin D revealed that the antibiotic binding to the resistant cells was lower by 70-75 per cent as compared to the cells of the susceptible strains. Gramicidin S impaired the intactness of the cytoplasmic membranes and increased the absorption of actinomycin D by the susceptible cells and to a much lesser extent by the cells of the resistant strains. Actinomycin D bound by the susceptible cells could not be washed out with a buffer solution. It could be separated from the cells only by extraction with an organic solvent. Comparative electron microscopy of the susceptible and resistant cells demonstrated that the cell walls in the resistant strains were 1.5-2-fold thicker than the cell walls in the susceptible strains. The actinomycin D resistance of the Staphylococcus strains resistant gramicidin S was likely conditioned by the barrier properties of the morphologically changed cell walls.

Absorption↗
PubMed1998

Mutation at either Arg336 or Arg562 in factor VIII is insufficient for complete resistance to activated protein C (APC)-mediated inactivation: implications for the APC resistance test.

Activated protein C (APC)-mediated inactivation of factor VIII (FVIII) correlates with cleavage at either Arg336 and/or Arg562. To elucidate the APC cleavage requirements for inactivation of FVIII, APC cleavage site mutants in FVIII (R336I, R562K and R336I/R562K) were made by site-directed mutagenesis. Analysis of these FVIII mutants expressed in COS-1 monkey cells demonstrated the thrombin-cleaved mutant R562K was resistant to APC cleavage at residue 562 but not at Arg336 and the thrombin cleaved mutant R3361 was mostly resistant to APC cleavage at residue 336, but was sensitive to APC cleavage at Arg562. The double mutant R336I/R562K was mostly resistant to cleavage at residue 336 and completely resistant to cleavage at residue 562. Thus, APC cleavage of FVIII does not require a specific order of cleavage at either residue. The functional inactivation by APC was studied using partially purified preparations of FVIII expressed in Chinese hamster ovary cells. Both single mutants were inactivated at similar rates but slower than wild-type FVIII, whereas the double mutant R336I/R562K was resistant to inactivation. The ability of a commercially available APC-resistance assay kit to detect APC resistant FVIII was tested by reconstituting FVIII deficient plasma with the APC resistant mutants. Only the R336I/R562K demonstrated a reduced APC-resistance ratio, indicating that this assay can not detect the single APC cleavage site mutant of FVIII. These results suggest that APC-mediated cleavage at either Arg336 or Arg562 partially inactivate FVIII.

Animals↗
PubMed1998

[Antibiotic resistance here to stay? Compensatory mutations restore virulence of resistant bacteria].

Bacterial antibiotic resistance has increased alarmingly because of overuse of antibiotics both in humans and animals. One way of reversing this development is to reduce the use of antibiotics, thus promoting the disappearance of the resistant bacteria already present in humans and the environment. This approach is based on the assumption that resistance is conferred at the cost of impaired survival fitness in the absence of antibiotics, as compared with sensitive strains. It seems to be generally true that resistant bacteria are less fit than the respective sensitive strains, which suggests that resistance may be reversible. However, a complicating factor is the frequent finding in resistant strains of various types of compensatory mutations that restore fitness without concomitant loss of resistance. Thus, second-site compensatory mutations may allow resistant strains to persist and compete successfully with sensitive strains even in an environment depleted of antibiotics. It is concluded in the article that, if compensatory mutations are as common in clinical settings as they are in the laboratory, many types of resistance will be irreversible.

Anti-Bacterial Agents↗
PubMed1996

Resistance to apoptosis of harringtonine-resistant HL60 cells induced by tetrandrine.

AIM: To study the mechanism of resistance to apoptosis in the harringtonine (Har)-resistant HL60 cells with tetrandrine (Tet). METHODS: Growth inhibition, flow cytometry, DNA agarose gel electrophoresis, protein phosphorylation, and RNA dot hybridization. RESULTS: The resistant cells had no cross resistance to Tet. Tet induced the sensitive but not the Har-resistant HL60 cells to apoptosis. The high phosphorylation of protein < 30 kDa occurred when the resistant cells were treated with Tet. Tet and Har increased the expression of c-myc mRNA in the sensitive HL60 cells. The expression of c-myc mRNA in the resistant cells was obviously decreased and almost not changed in treatment with Tet and Har. CONCLUSION: Tet induced the sensitive but not the Har-resistant HL60 cells to apoptosis, and the resistance to apoptosis induced by Tet was associated with the high protein phosphorylation and reduction of the expression of c-myc mRNA.

Alkaloids↗
PubMed2026

Molecular Diagnostics for WHO Priority Bacterial Pathogens: A Bibliometric Mapping of Diagnostic Platforms, Resistance Markers, and Antimicrobial Resistance Research Trends.

Antimicrobial resistance (AMR) constrains effective treatment and carries implications for infection control, surveillance, and public health. The World Health Organization (WHO) priority bacterial pathogen framework has intensified the need for diagnostic innovation by redefining research priorities around organisms combining high disease burden with complex resistance profiles. Molecular diagnostics have accordingly moved beyond culture-based workflows, integrating rapid pathogen identification, resistance-marker detection, genomic surveillance, and clinical decision support. The present study conducted a bibliometric mapping of the literature on WHO priority pathogens. Rather than addressing resistance at a general level or a single pathogen or technology, it integrates priority pathogens, molecular platforms, and resistance markers within a single framework, tracing their joint thematic and temporal evolution along an explicit pathogen-platform-marker axis. Scopus-indexed articles and reviews (2000-2025) were retrieved, yielding 1746 publications after screening adapted from the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Analyses used Bibliometrix/Biblioshiny, R, and VOSviewer. The literature expanded markedly after 2018, led by China and the United States. Methicillin-resistant Staphylococcus aureus (MRSA), Mycobacterium tuberculosis, Enterococcus faecium, and the Enterobacterales-carbapenemase axis constituted the principal thematic cores, whereas conventional polymerase chain reaction (PCR)/nucleic acid amplification testing (NAAT) and whole-genome sequencing were the dominant platforms. Overall, the field has evolved from pathogen detection into an AMR-centered translational domain encompassing resistance prediction, genomic epidemiology, surveillance, and clinical decision support. Diagnostic development, stewardship, and surveillance depend on hybrid workflows coupling rapid marker-targeted assays with genome-based characterization, delivering actionable resistance within clinically meaningful timeframes, and extending coverage to underrepresented pathogens and platforms.

Humans↗
PubMed1998

Activated cell-wall synthesis is associated with vancomycin resistance in methicillin-resistant Staphylococcus aureus clinical strains Mu3 and Mu50.

We have previously reported methicillin-resistant Staphylococcus aureus clinical strains, Mu50 and Mu3, representing two categories of vancomycin resistance: Mu50 representing vancomycin-resistant S. aureus (VRSA) with MICs > or = 8 mg/L, and Mu3 representing hetero-VRSA with MICs < or = 4 mg/L using standard MIC determination methods. The mechanisms of vancomycin resistance in these strains were investigated. These strains did not carry the enterococcal vancomycin-resistance genes, vanA, vanB, or vanC1-3, as tested by PCR using specific primers. However, both strains produced three to five times the amount of penicillin-binding proteins (PBPs) 2 and 2' when compared with vancomycin-susceptible S. aureus control strains with or without methicillin resistance; the amounts of PBP2 produced in Mu3 and Mu50 were comparable to those in the vancomycin-resistant S. aureus mutant strains selected in vitro. Incorporation of 14C-labelled Nacetyl-glucosamine into the cell was three to 20 times increased in Mu50 and Mu3, and release of the radioactive cell wall material was increased in Mu3 (and also in Mu50, though to a lesser extent), compared with control strains. The amounts of intracellular murein monomer precursor in these strains were three to eight times greater than those found in control strains. Transmission electron microscopy showed a doubling in the cell wall thickness in Mu50 compared with the control strains. Mu3 did not show obvious cell wall thickening. These data indicate that activated synthesis and an increased rate of cell wall turnover are common features of Mu3 and Mu50 and may be the prerequisite for the expression of vancomycin resistance in S. aureus.

Acetylglucosamine↗
PubMed2003

Cross-resistance and associated resistance in 2478 Escherichia coli isolates from the Pan-European ECO.SENS Project surveying the antimicrobial susceptibility of pathogens from uncomplicated urinary tract infections.

The antimicrobial resistance profiles, comprising 12 antibiotics, of 2478 isolates of Escherichia coli from the ECO.SENS Project involving women with acute uncomplicated urinary tract infection at 252 community health care centres in 17 countries were determined. Resistance to ampicillin alone (6.3%) and sulfamethoxazole alone (5.4%) were the most common 'single resistances'. Multiple resistance was most common in Spain and least common in Finland. The main associated-resistance profiles involved ampicillin/sulfamethoxazole (8.7%) and ampicillin/sulfamethoxazole/trimethoprim/trimethoprim-sulfamethoxazole (6.4%). The most common profile of multiple resistance was ampicillin/sulfamethoxazole/trimethoprim/trimethoprim-sulfamethoxazole/nalidixic acid/ciprofloxacin. Twenty-one isolates, half of which came from Spain, were resistant to seven antibiotics or more. Three isolates, one from Spain and two from Portugal, were resistant to nine of the 12 antibiotics investigated.

Ampicillin Resistance↗
PubMed1999

Increase in incidence of resistance to ampicillin, chloramphenicol and trimethoprim in clinical isolates of Salmonella serotype Typhimurium with investigation of molecular epidemiology and mechanisms of resistance.

Antimicrobial resistance patterns of Salmonella serotype Typhimurium isolates obtained during the period 1987-1994 were examined and the molecular epidemiology and the mechanisms of resistance to ampicillin, chloramphenicol and trimethoprim were investigated in 24 strains isolated during 1994. Resistance to ampicillin increased from 18% to 78%, to chloramphenicol from 15% to 78%, to tetracycline from 53% to 89% and to co-trimoxazole from 3% to 37%, whereas resistance to norfloxacin remained at 0%. Of Salmonella serotype Typhimurium strains isolated during 1994, all ampicillin-resistant strains had an MIC > 256 mg/L, except one strain in which the MIC was 64 mg/L. Twelve strains (52%) had a TEM-type beta-lactamase, nine (39%) a CARB-type beta-lactamase and two strains (8%) had an OXA-type beta-lactamase. Chloramphenicol acetyl-transferase activity was detected in only nine (47%) of 19 chloramphenicol resistant strains, whereas all eight trimethoprim-resistant strains produced a dihydrofolate reductase type Ia enzyme. Three different epidemiological groups were defined by either low-frequency restriction analysis of chromosomal DNA and pulsed-field gel electrophoresis or repetitive extragenic palindromic-PCR. The latter technique provided an alternative, rapid and powerful genotyping method for S. Typhimurium. Although quinolones provide a good therapeutic alternative, the multiresistance of S. Typhimurium is of public health concern and it is important to continue surveillance of resistance levels and their mechanisms.

Ampicillin Resistance↗