Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “resistant”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 901 records · Page 50Linked to original sources
PubMed2001

Changing pattern of antibiotic resistance in methicillin-resistant Staphylococcus aureus from German hospitals.

OBJECTIVE: To investigate the background of changes of resistance phenotypes in methicillin-resistant Staphylococcus aureus (MRSA) from nosocomial infections in German hospitals by molecular typing and identification of particular resistance genes. METHODS: Isolates from the network for monitoring the spread of MRSA in Germany were subjected to quantitative susceptibility testing, to molecular typing, and to polymerase chain reaction identification of resistance genes. PARTICIPANTS: The network consists of 175 German clinical microbiological laboratories collaborating with the German Reference Center for Staphylococci, which performs typing of staphylococcal isolates from nosocomial infections and data analysis. RESULTS: During the past 5 years, MRSA susceptible to other antibiotics such as oxytetracycline, erythromycin, and gentamicin became more frequent. The proportion of epidemic MRSA clones that had been disseminated in the past and that exhibited broad resistance phenotypes decreased, whereas the proportion of recently emerging MRSA carrying only a few other resistance determinants has increased (1994, 11.5%; 1998, 39%). CONCLUSIONS: The changing pattern of resistance phenotypes of MRSA from nosocomial infections in Germany is mainly due to the spread of recently emerging epidemic strains that are less frequently resistant to antibacterials other than oxacillin. The observed changes cannot simply be attributed to overall antibiotic consumption.

Anti-Bacterial Agents↗
PubMed2006

Descriptive epidemiology and case-control study of patients colonized with vancomycin-resistant enterococcus and methicillin-resistant Staphylococcus aureus.

BACKGROUND: Patients colonized or infected with vancomycin-resistant enterococcus and methicillin-resistant Staphylococcus aureus may be at risk of acquiring vancomycin-resistant S. aureus if the vanA gene is transferred from vancomycin-resistant enterococcus to methicillin-resistant S. aureus. OBJECTIVE: Our goal was to identify risk factors for cocolonization or coinfection (CC/CI) with vancomycin-resistant enterococcus and methicillin-resistant S. aureus. DESIGN: We conducted a descriptive, epidemiologic study of all patients with CC/CI identified from January 1998 to May 2003 and a nested case-control study of a cohort of patients hospitalized in the burn and wound unit. SETTING: We conducted our study in a 813-bed tertiary care university teaching hospital. POPULATION: The study population consisted of patients found to have CC/CI during the study period. METHODS: Descriptive epidemiologic data were collected from hospital records of all patients identified as having CC/CI. A subset of patients hospitalized in the burn and wound unit were included in a case-control study. RESULTS: CC/CI was detected in 71% of the patients during a single hospital stay. The burn and wound unit, which does active surveillance for both organisms, and the general medicine unit, which does not do active surveillance for either organism, cared for more than one-half of these patients. Among patients being cared for in the burn and wound unit, having exposure to 2 or more invasive devices (central venous catheters, indwelling urinary catheters, and enteral feeding tubes) and renal insufficiency were independent risk factors for CC/CI. CONCLUSIONS: Patients with CC/CI are the population at greatest risk for vancomycin-resistant S. aureus colonization or infection. The number of invasive devices to which patients are exposed and, thus, possibly the patients' underlying severity of illness, as well as renal insufficiency, appear to be risk factors for CC/CI.

Adult↗
PubMed2004

Distribution of the erm (B) gene, tetracycline resistance genes, and Tn1545-like transposons in macrolide- and lincosamide-resistant enterococci from pigs and humans.

The distribution of the erm (B) and the tetracycline resistance genes tet(K), tet(L), tet(M), tet(O), and tet(S) was investigated among macrolide- and lincosamide-resistant enterococci originating from humans, pigs, and pork carcasses. The presence of transposons of the Tn916/Tn1545 family was also traced in these isolates. Furthermore, the porcine strains were tested for the presence of glycopeptide resistance genes vanA and vanB. The erm(B) gene was found in 85% of the porcine and in all human isolates. Ninety-eight percent of the porcine and 89% of the human erm(B)-positive enterococci carried the tet(M) gene. Seventy-seven percent and 70%, respectively, of these strains harbored a Tn1545-like element. Tet(L) was observed in 68% of the porcine and in 65% of the human enterococci. The other tetracycline resistance genes were very rare and the glycopeptide resistance genes vanA and vanB were not detected among the porcine isolates. The similar frequencies of resistance genes and the highly mobile Tn1545-like transposon among porcine and human enterococci might indicate exchange of resistant strains or their resistance genes between humans and pigs or the existence of a common reservoir.

Animals↗
PubMed1999

Markedly different rates and resistance profiles exhibited by seven commonly used and newer beta-lactams on the selection of resistant variants of Enterobacter cloacae.

Seven beta-lactam antibiotics (cefepime, cefoperazone, ceftazidime, ceftriaxone, cefamandole, imipenem and meropenem) were tested for their potential to select resistance in standard and clinical strains of Enterobacter cloacae (n = 9). The strains were subcultured daily with the test antibiotics at doubling concentrations starting at 0.125 x MIC. Development of resistance throughout the passages was detected by a disc diffusion test. Ceftazidime, ceftriaxone and cefamandole selected resistance at a faster rate than cefoperazone, cefepime and meropenem. Imipenem did not select resistance in the nine strains tested and was the only antibiotic that eradicated all the strains during selection. The resistance patterns of strains selected by meropenem, cefepime and the other cephalosporins were markedly different, although cross-resistance to the early generation cephalosporins was common. The resistance phenotypes of most strains remained stable upon serial passages in antibiotic-free medium. The findings of this study highlight the importance of the choice of antibiotic for therapy not only on the basis of its antibacterial activity, but also on its potential to select resistance to itself and other antibiotics.

Anti-Bacterial Agents↗
PubMed2002

Antibiotic resistance: effect of different criteria for classifying isolates as duplicates on apparent resistance frequencies.

OBJECTIVE: To investigate the effect of screening specimens and different criteria for exclusion of duplicate isolates when surveillance of antimicrobial resistances is performed. MATERIALS AND METHODS: Trends in resistance were analysed for recent isolates of selected organisms from Guy's and St Thomas' Hospitals with the use of various criteria for the exclusion of duplicates, including time since the last isolate and antibiogram pattern, and the effect of excluding screening specimens. RESULTS: There was a significant difference of about 8% in the apparent frequency of methicillin resistance in Staphylococcus aureus in inpatients if the time limit for duplicates was set at 5 rather than 30 days; it was about 10% if a 5 day limit was compared with a 365 day limit. There was also a significant difference, of 6-10%, in apparent resistance frequencies if isolates from screening specimens were excluded. Apparent gentamicin resistance rates in Klebsiella spp. varied between 11% and 28%, and the number of apparent patient isolates of gentamicinresistant organisms varied by up to 35%, depending on the duplicate exclusion criteria chosen. Effects were smaller, though still significant, for vancomycin resistance in Enterococcus spp. There was little effect for amoxicillin or cefuroxime resistance in Escherichia coli isolates from general practitioners, where the proportion of duplicates was small. CONCLUSION: Improved surveillance of antibiotic resistance is needed. However, care needs to be taken in setting the criteria for classifying isolates as duplicates and in comparing results where these criteria may be different or unknown.

Bacteria↗
PubMed1999

Multidrug resistance and the lung resistance-related protein in human colon carcinoma SW-620 cells.

BACKGROUND: Lung resistance-related protein (LRP), the major vault protein in humans, is sometimes overexpressed in multidrug-resistant cells. Because cells transfected with the LRP gene did not express the multidrug-resistant phenotype, we investigated whether LRP is involved in multidrug resistance. METHODS: SW-620 cells, a human colon carcinoma cell line, alone or transfected with an expression vector carrying a LRP-specific ribozyme or with an empty vector, were treated with sodium butyrate to induce differentiation. Expression of P-glycoprotein, multidrug resistance protein, and LRP in the cells was examined by northern and western blotting, and the efflux of doxorubicin in the cells or isolated nuclei was examined by fluorescence microscopy. RESULTS: A 2-week treatment with sodium butyrate induced LRP and conferred resistance to doxorubicin, vincristine, etoposide, gramicidin D, and paclitaxel (Taxol) in SW-620 cells. Insertion of either of two LRP-specific ribozymes into SW-620 cells inhibited these activities. Levels of drugs accumulating in the cells were not decreased by sodium butyrate, suggesting that the adenosine triphosphate-binding cassette transporter is not involved in sodium butyrate-induced multidrug resistance. Doxorubicin was mainly located in the nuclei of untreated cells and in the cytoplasm of sodium butyrate-treated cells. Isolated nuclei from untreated cells or sodium butyrate-treated cells incubated with anti-LRP polyclonal antibodies contained more doxorubicin than the nuclei of sodium butyrate-treated cells alone. Efflux of doxorubicin was greater from the nuclei of sodium butyrate-treated cells than the nuclei of untreated cells or of sodium butyrate-treated cells transfected with a LRP-specific ribozyme and was inhibited by an anti-LRP polyclonal antibody. CONCLUSIONS: LRP is involved in resistance to doxorubicin, vincristine, etoposide, paclitaxel, and gramicidin D and has an important role in the transport of doxorubicin from the nucleus to the cytoplasm.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Atypical multidrug resistance: breast cancer resistance protein messenger RNA expression in mitoxantrone-selected cell lines.

BACKGROUND: Human cancer cell lines grown in the presence of the cytotoxic agent mitoxantrone frequently develop resistance associated with a reduction in intracellular drug accumulation without increased expression of the known drug resistance transporters P-glycoprotein and multidrug resistance protein (also known as multidrug resistance-associated protein). Breast cancer resistance protein (BCRP) is a recently described adenosine triphosphate-binding cassette transporter associated with resistance to mitoxantrone and anthracyclines. This study was undertaken to test the prevalence of BCRP overexpression in cell lines selected for growth in the presence of mitoxantrone. METHODS: Total cellular RNA or poly A+ RNA and genomic DNA were isolated from parental and drug-selected cell lines. Expression of BCRP messenger RNA (mRNA) and amplification of the BCRP gene were analyzed by northern and Southern blot hybridization, respectively. RESULTS: A variety of drug-resistant human cancer cell lines derived by selection with mitoxantrone markedly overexpressed BCRP mRNA; these cell lines included sublines of human breast carcinoma (MCF-7), colon carcinoma (S1 and HT29), gastric carcinoma (EPG85-257), fibrosarcoma (EPF86-079), and myeloma (8226) origins. Analysis of genomic DNA from BCRP-overexpressing MCF-7/MX cells demonstrated that the BCRP gene was also amplified in these cells. CONCLUSIONS: Overexpression of BCRP mRNA is frequently observed in multidrug-resistant cell lines selected with mitoxantrone, suggesting that BCRP is likely to be a major cellular defense mechanism elicited in response to exposure to this drug. It is likely that BCRP is the putative "mitoxantrone transporter" hypothesized to be present in these cell lines.

Antineoplastic Agents↗
PubMed1999

What can be learnt from the new data about antibiotic resistance? Are there any practical clinical consequences of Helicobacter pylori antibiotic resistance?

Effective treatment regimens are now available for the eradication of Helicobacter pylori, but one of the factors limiting their efficacy is antibiotic resistance. Omeprazole-based triple therapy (omeprazole plus two antibiotics) can, at present, be considered the treatment of choice for H. pylori infection; some of the best results have been achieved by combining omeprazole with either amoxycillin and clarithromycin or metronidazole and clarithromycin. However, the potential effectiveness of nitroimidazole derivatives and clarithromycin must be weighed against the possibility that resistance can develop to these agents. Eradication in metronidazole-resistant strains is lower than in sensitive strains, but is still about 75% (versus 97%). However, clarithromycin resistance is thought to have more clinical significance, reducing the eradication rate of 95% in sensitive strains to 40% in resistant strains, although the overall importance of clarithromycin resistance for H. pylori eradication is still likely to be relatively low. Recent data on secondary resistance indicate that the rate is at least 50% for both metronidazole and clarithromycin in patients in whom eradication has failed. If, in the future, a large number of H. pylori-positive individuals undergo such treatment, treatment failures may become a major issue, and the problem of antibiotic resistance will have to be overcome.

Anti-Bacterial Agents↗
PubMed1998

Analysis of neomycin, kanamycin, tobramycin and amikacin resistance mechanisms in gentamicin-resistant isolates of Enterobacteriaceae.

Twenty-four gentamicin-resistant isolates of Enterobacteriaceae, obtained from the clinical laboratories of three health centres in Nablus, Palestine, were tested for susceptibility to neomycin, kanamycin, tobramycin and amikacin. Resistance rates were 29.2% for neomycin, 58.3% for kanamycin, 45.8% for tobramycin and 8.3% for amikacin. Fourteen (58.3%) isolates were noted to be multiresistant, i.e., resistant to gentamicin and two or more other aminoglycosides; resistance to gentamicin, kanamycin and tobramycin was the most common pattern of multiple resistance. This pattern implies the involvement of adenyltransferase ANT(")-I activity. Plasmid profiles and curing experiments suggested a plasmid localisation of gentamicin, neomycin, kanamycin and tobramycin resistance genes. However, a chromosomal location is proposed for plasmid-deficient strains. Cross-resistance in two isolates to all aminoglycosides tested suggested membrane impermeability to aminoglycosides as the mechanism of resistance.

Amikacin↗
PubMed2004

Characterization of an inducible vancomycin resistance system in Streptomyces coelicolor reveals a novel gene (vanK) required for drug resistance.

Vancomycin is the front-line therapy for treating problematic infections caused by methicillin-resistant Staphylococcus aureus (MRSA), and the spread of vancomycin resistance is an acute problem. Vancomycin blocks cross-linking between peptidoglycan intermediates by binding to the D-Ala-D-Ala termini of bacterial cell wall precursors, which are the substrate of transglycosylase/transpeptidase. We have characterized a cluster of seven genes (vanSRJKHAX) in Streptomyces coelicolor that confers inducible, high-level vancomycin resistance. vanHAX are orthologous to genes found in vancomycin-resistant enterococci that encode enzymes predicted to reprogramme peptidoglycan biosynthesis such that cell wall precursors terminate in D-Ala-D-Lac rather than D-Ala-D-Ala. vanR and vanS encode a two-component signal transduction system that mediates transcriptional induction of the seven van genes. vanJ and vanK are novel genes that have no counterpart in previously characterized vancomycin resistance clusters from pathogens. VanK is a member of the Fem family of enzymes that add the cross-bridge amino acids to the stem pentapeptide of cell wall precursors, and vanK is essential for vancomycin resistance. The van genes are organized into four transcription units, vanRS, vanJ, vanK and vanHAX, and these transcripts are induced by vancomycin in a vanR-dependent manner. To develop a sensitive bioassay for inducers of the vancomycin resistance system, the promoter of vanJ was fused to a reporter gene conferring resistance to kanamycin. All the inducers identified were glycopeptide antibiotics, but teicoplanin, a membrane-anchored glycopeptide, failed to act as an inducer. Analysis of mutants defective in the vanRS and cseBC cell envelope signal transduction systems revealed significant cross-talk between the two pathways.

Amino Acid Sequence↗
PubMed2003

Breast cancer resistance protein (BCRP/ABCG2) induces cellular resistance to HIV-1 nucleoside reverse transcriptase inhibitors.

Breast cancer resistance protein (BCRP/ABCG2) is a novel member of ATP- binding cassette transporters, which induce multidrug resistance in cancer cells. We found that a high level of BCRP expression in CD4+ T cells conferred cellular resistance to human immunodeficiency virus type-1 (HIV-1) nucleoside reverse transcriptase inhibitors. The cell line MT-4/DOX 500 was established through the long-term culture of MT-4 cells in the presence of doxorubicin (DOX) and had reduced sensitivity to not only DOX but also zidovudine (AZT). MT-4/DOX 500 cells showed reduced intracellular accumulation and retention of DOX and increased ATP-dependent rhodamine 123 efflux. The cells were also resistant to several anticancer agents such as mitoxantrone, 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin, and 7-ethyl-10-hydroxycamptothecin. AZT was 7.5-fold less inhibitory to HIV-1 replication in MT-4/DOX 500 cells than in MT-4 cells. Furthermore, the anti-HIV-1 activity of lamivudine was severely impaired in MT-4/DOX 500 cells. In contrast, the antiviral activity of non-nucleoside reverse transcriptase inhibitors and protease inhibitors was not affected in the cells. MT-4/DOX 500 cells expressed glycosylated BCRP but not P-glycoprotein (ABCB1), multidrug resistance protein 1, 2, or 4 (ABCC1, -2, or -4), or lung resistance-related protein. In addition, the BCRP-specific inhibitor fumitremorgin C completely abolished the resistance of MT-4/DOX 500 cells to AZT as well as to DOX. An analysis for intracellular metabolism of AZT suggests that the resistance is attributed to the increase of ATP-dependent efflux of its metabolites, presumably AZT 5'-monophosphate, in MT-4/DOX 500 cells.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2003

Epidemiology of nalidixic acid resistance and TEM-1- and TEM-52-mediated ampicillin resistance of Shigella sonnei isolates obtained in Korea between 1980 and 2000.

The resistance to ampicillin and nalidixic acid in Shigella sonnei isolates obtained in Korea during the period 1998 to 2000 was characterized. Recently (J. Y. Oh, H. S. Yu, S. K. Kim, S. Y. Seol, D. T. Cho, and J. C. Lee, J. Clin. Microbiol. 41:421-423, 2003) ampicillin and nalidixic acid resistance was found in 49 and 70%, respectively, of the 67 S. sonnei isolates obtained during this period. We analyzed 138 S. sonnei isolates collected during the same period. Ampicillin and nalidixic acid resistance was found in 30 and 86% of the isolates, respectively. The ampicillin resistance was mediated by a TEM-1 beta-lactamase, and TEM-52 extended-spectrum beta-lactamase was identified in one sporadic S. sonnei isolate from 1999. bla(TEM-1) and bla(TEM-52) were located in conjugative R-plasmids. Tn3 was detected in 41% of the ampicillin-resistant isolates. The R-plasmids from the transconjugants that transferred resistance to ampicillin exhibited different restriction fragment length polymorphism patterns, and a bla(TEM-1) probe was hybridized with the different fragments. The nalidixic acid resistance was exclusively associated with an amino acid substitution, Ser83-->Leu (TCG-->TTG), in gyrA. These findings indicate that the genetically related S. sonnei strains readily acquire resistance to ampicillin, streptomycin, trimethoprim, and sulfamethoxazole but not nalidixic acid through conjugative R-plasmids from difference sources when confronted by antibiotic selective pressures.

Ampicillin Resistance↗
PubMed1963

EPISOME-MEDIATED TRANSFER OF DRUG RESISTANCE IN ENTEROBACTERIACEAE. VI. HIGH-FREQUENCY RESISTANCE TRANSFER SYSTEM IN ESCHERICHIA COLI.

Watanabe, Tsutomu (Keio University, Tokyo, Japan). Episome-mediated transfer of drug resistance in Enterobacteriaceae. VI. High-frequency resistance transfer system in Escherichia coli. J. Bacteriol. 85:788-794. 1963.-R-factors (transmissible drug-resistance factors composed of the resistance-transfer factor and markers of resistance to sulfonamide, streptomycin, chloramphenicol, and tetracycline) gave rise to a high-frequency transfer system in Escherichia coli K-12 F(-), F(+), and Hfr strains that was similar to the high-frequency colicinogeny transfer system (HFCT) found by Stocker and Ozeki in Salmonella typhimurium with colicinogenic factor I. The procedure for obtaining a high-frequency transfer system of R-factors was identical to that for HFCT. The majority of cells of the high-frequency resistance transfer system were composed of cells which had just received R-factors by conjugation. These cells could act as highly competent donor cells for further transfer of the R-factors by conjugation. The frequencies of transfer of R-factors were as high as 1.5 to 7.5 per resistant donor cell introduced into mixed incubation with drug-sensitive recipient cells for 1 hr at 37 C, whereas the usual donor cells could transfer the R-factors at frequencies of, at most, 1:30 under similar conditions of mixed cultivation. It was also found that the aerobic conditions for growth of donor cells rather reduced the frequencies of transfer of R-factors in the usual systems. Possible mechanisms of the high-frequency resistance transfer system are discussed.

Anti-Bacterial Agents↗
PubMed1964

RESISTANCE AND CROSS-RESISTANCE OF ESCHERICHIA COLI S MUTANTS TO THE RADIOMIMETIC AGENT PROFLAVINE.

Woody-Karrer, Pearl (Palo Alto Medical Research Foundation, Palo Alto, Calif.), and Joseph Greenberg. Resistance and cross-resistance of Escherichia coli S mutants to the radiomimetic agent proflavine. J. Bacteriol. 87:536-542. 1964.-All 50 of the first-step mutants of Escherichia coli S selected for resistance to proflavine were resistant to ultraviolet light and each of five different radiomimetic chemicals. The mutants were classified into eight types on the basis of their relative resistance to six different radiomimetic drugs and on the basis of the shape of their ultraviolet survival curves. Three of these types are identical to types previously isolated with other radiomimetic drugs; five of the types are new. A high proportion of the clones surviving proflavine treatment were phenotypically but not genetically resistant, and no strains were isolated which were resistant to proflavine but were not resistant to radiation.

Acridines↗
PubMed2005

Relationship between the original multiply resistant South African isolates of Streptococcus pneumoniae from 1977 to 1978 and contemporary international resistant clones.

High-level penicillin G-resistant as well as multidrug-resistant Streptococcus pneumoniae isolates were first described in South Africa in 1977. The relationship between these original multidrug-resistant South African isolates and other resistant clones was investigated. Twenty-six representative isolates isolated from initial outbreaks in South Africa from 1977 to 1978 were characterized by multilocus sequence typing and pulsed-field gel electrophoresis. Twenty-one isolates were penicillin resistant and five were penicillin intermediate, with variable susceptibilities to macrolides, clindamycin, chloramphenicol, tetracycline, and trimethoprim-sulfamethoxazole. Fourteen isolates were serotype 19A, 11 were serotype 6A, and one was serotype 14. Penicillin-resistant serotype 19A isolates belonged to three closely related sequence types (STs), ST 41 (n = 6), ST 1605 (n = 3), and ST 1656 (n = 1). Penicillin-resistant serotype 6A isolates belonged to two closely related STs, ST 1094 (n = 10) and ST 1607 (n = 1), and were not closely related to other international clones. The serotype 14 penicillin-intermediate isolate was not closely related to the other isolates from South Africa but was a predicted founder of a clonal group with 41 different STs. Five new STs, ST 1605, ST 1607, ST 1608, ST 1610, and ST 1656, are described for the first time in this study. New molecular methods have characterized the original multiply resistant South African pneumococcal isolates from 1977 to 1978 and have shown the relationships of these clones to major pneumococcal clones.

Anti-Bacterial Agents↗
PubMed2003

Survey of high- and low-level mupirocin-resistant strains of methicillin-resistant Staphylococcus aureus in 15 Japanese hospitals.

BACKGROUND: The extent of mupirocin-resistant methicillin-resistant Staphylococcus aureus (MRSA) in countries using mupirocin only for the eradication of nasal carriage of MRSA is unknown. METHODS: During 1997, 1998, 1999, 2000, and 2001, 1368 strains of MRSA were isolated from 15 general hospitals in the Tohoku area of Japan and tested for susceptibility to mupirocin. RESULTS: The isolation of low-level mupirocin resistance was 0.8% in 1997, 1.1% in 1998, 0.7% in 1999, 4.0% in 2000, and 2.4% in 2001. For the first 3 years it was about 1%. However, the isolation rate of low-level mupirocin resistance in MRSA increased dramatically in 2000. High-level mupirocin resistance was not detected during these years. CONCLUSION: Most patients from whom low-level mupirocin resistant MRSA were found in 2000 and 2001 had previously received mupirocin treatment for eradicating nasal carriage of MRSA, and these strains were isolated from sputum or the pharynx. This result indicates that mupirocin treatment is likely to be one of the causes of mupirocin resistance and, therefore, the development of low-level mupirocin resistance in MRSA isolated from sputum or the pharynx should be considered when using mupirocin in order to improve the control of the spread of MRSA in hospitals.

Anti-Bacterial Agents↗
PubMed2006

Antibacterial resistance and molecular typing of methicillin-resistant Staphylococcus aureus in a Kuwaiti general hospital.

OBJECTIVE: To investigate antibiotic resistance and genetic relatedness of methicillin-resistant Staphylococcus aureus (MRSA) isolated in a general hospital in Kuwait over a period from 1996 to 1998 and 2001. MATERIAL AND METHODS: The isolates were characterized by antibacterial susceptibility testing, coagulase serotyping, coagulase gene polymorphism (coag-RFLP) and pulsed-field gel electrophoresis (PFGE). RESULTS: The MRSA isolates were highly resistant to gentamicin, kanamycin, ciprofloxacin, tetracycline, fusidic acid and mupirocin. The prevalence of gentamicin, kanamycin, streptomycin, tetracycline and erythromycin resistance remained high (80-96%) throughout the study period, but the prevalence of resistance to ciprofloxacin, fusidic acid and mupirocin steadily increased. The already high mupirocin resistance level increased from 12.5 in 1996, to 85.7% in 2001, and the fusidic acid resistance varied between 70.8 and 85.7%. In contrast, chloramphenicol and trimethoprim resistance declined from 25 and 29% in 1996 to 4.7 and 14.2% in 2001, respectively. The majority (91.5%) of the isolates were coagulase serotype 4. AluI restriction endonuclease analysis of amplified coagulase gene generated four coag-RFLP patterns: 92% of them were coag-RFLP type 1, while types 2, 3 and 4 were 3.5, 4.6 and 1.1% respectively. PFGE differentiated them into seven pulsotypes (PFGE types 1-7). The PFGE type 1 pulsotype constituted 90.2% of the isolates. Isolates with the type A coag-RFLP also had the type1 PFGE pulsotypes. CONCLUSION: The concordant results of PFGE and coag-RFLP demonstrated the presence of a persistent MRSA clone in the hospital during the study period.

Anti-Bacterial Agents↗
PubMed2001

Sub-inhibitory concentrations of vancomycin prevent quinolone-resistance in a penicillin-resistant isolate of Streptococcus pneumoniae.

BACKGROUND: The continuous spread of penicillin-resistant pneumococci represents a permanent threat in the treatment of pneumococcal infections, especially when strains show additional resistance to quinolones. The main objective of this study was to determine a treatment modality impeding the emergence of quinolone resistance. RESULTS: Exposure of a penicillin-resistant pneumococcus to increasing concentrations of trovafloxacin or ciprofloxacin selected for mutants resistant to these drugs. In the presence of sub-inhibitory concentrations of vancomycin, development of trovafloxacin-resistance and high-level ciprofloxacin-resistance were prevented. CONCLUSIONS: Considering the risk of quinolone-resistance in pneumococci, the observation might be of clinical importance.

4-Quinolones↗