scholarly journals High-level resistance to trimethoprim in Shigella sonnei associated with plasmid-encoded dihydrofolate reductase type I.

1988 ◽  
Vol 32 (10) ◽  
pp. 1598-1599 ◽  
Author(s):  
R Delgado ◽  
J R Otero
1992 ◽  
Vol 109 (3) ◽  
pp. 453-462 ◽  
Author(s):  
Lin-Li Chang ◽  
Shui-Feng Chang ◽  
Teh-Yuan Chow ◽  
Wen-Jeng Wu ◽  
Jong-Chou Chang

SUMMARYBetween July 1987 and June 1989, 1054 urinary isolates of enterobacteria from Kaohsiung, Taiwan were studied for their trimethoprim resistance. Trimethoprim resistance was defined as MIC greater than 4 μg/ml and high-level resistance by MIC greater than 1000 μg/ml. The incidence of trimethoprim resistance increased from 33·6% in 1987 to 42·1% in 1989. Among the resistant strains studied, 90% were resistant to high levels of trimethoprim. An increase in the proportion of resistant strains (33·9–46·3%) exhibiting high-level non-transferable trimethoprim resistance was noted. The distribution of the dihydrofolate reductase (DHFR) genes by colony hybridization in 374 trimethoprim-resistant isolates revealed the presence of type I and type V DHFR genes in most of these isolates (45·4% and 10·4% respectively). Type I was predominant inEscherichia coliwhereas type V was frequently seen inEnterobacterspp. None showed homology with the type II and type III DHFR probe DNA. In addition, transposon Tn7 was present in 7·8% of 374 trimethoprim-resistant enterobacteria.


1988 ◽  
Vol 22 (4) ◽  
pp. 429-435 ◽  
Author(s):  
B. A. Wylie ◽  
S. G. B. Amyes ◽  
H.-K. Young ◽  
H. J. Koornhof

1975 ◽  
Vol 25 (3) ◽  
pp. 207-214 ◽  
Author(s):  
A. S. Breeze ◽  
P. Sims ◽  
K. A. Stacey

SUMMARYTrimethoprim-resistant mutants ofE. coliK12 have been isolated by-serial subculture in progressively higher concentrations of trimethoprim. High-level resistance depends on the accumulation of several mutational changes. Transduction with bacteriophage P1 has shown that all the mutations involved in resistance are associated with a locus, to be calledtmr, betweenpyr AandpdxAand closely linked topdxA. Resistance is accompanied by, and presumably due to, an increased activity of the target enzyme, dihydrofolate reductase. Thetmrlocus may include the structural gene for dihydrofolate reductase but the only mutations that have so far been observed are concerned with regulation.


1997 ◽  
Vol 41 (5) ◽  
pp. 1134-1136 ◽  
Author(s):  
E Charpentier ◽  
P Courvalin

The sequence of the trimethoprim resistance gene of the 3.7-kb plasmid (pIP823) that confers high-level resistance (MIC, 1,024 microg/ml) to Listeria monocytogenes BM4293 was determined. The gene was identical to dfrD recently detected in Staphylococcus haemolyticus MUR313. The corresponding protein, S2DHFR, represents the second class of high-level trimethoprim-resistant dihydrofolate reductase identified in gram-positive bacteria. We propose that trimethoprim resistance in L. monocytogenes BM4293 could originate in staphylococci.


1996 ◽  
Vol 40 (3) ◽  
pp. 581-585 ◽  
Author(s):  
J L Pernodet ◽  
S Fish ◽  
M H Blondelet-Rouault ◽  
E Cundliffe

Genes conferring resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics via ribosomal modification are widespread in bacteria, including clinical isolates and MLS-producing actinomycetes. Such erm-type genes encode enzymes that mono- or dimethylate residue A-2058 of 23S rRNA. The different phenotypes resulting from monomethylation (MLS-I phenotype, conferred by erm type I genes) or dimethylation (MLS-II phenotype due to erm type II genes) have been characterized by introducing tlrD or ermE, respectively, into an MLS-sensitive derivative of Streptomyces lividans TK21. This strain (designated OS456) was generated by specific replacement of the endogenous resistance genes lrm and mgt. The MLS-I phenotype is characterized by high-level resistance to lincomycin with only marginal resistance to macrolides such as chalcomycin or tylosin, whereas the MLS-II phenotype involves high-level resistance to all MLS drugs. Mono- and dimethylated ribosomes were introduced into a cell-free protein-synthesizing system prepared from S. lividans and compared with unmodified particles in their response to antibiotics. There was no simple correlation between the relative potencies of MLS drugs at the level of the target site (i.e., the ribosome) and their antibacterial activities expressed as MICs.


2010 ◽  
Vol 82 (4) ◽  
pp. 535-541 ◽  
Author(s):  
Amani Kheir ◽  
Yagut Akbarova ◽  
Salma Al-Saai ◽  
Göte Swedberg ◽  
Hamza A. Babiker ◽  
...  

1999 ◽  
Vol 37 (6) ◽  
pp. 1913-1920 ◽  
Author(s):  
Raquel Sá-Leão ◽  
Ilda Santos Sanches ◽  
Dora Dias ◽  
Isabel Peres ◽  
Rosa M. Barros ◽  
...  

Close to half of the 878 methicillin-resistant Staphylococcus aureus (MRSA) strains recovered between 1992 and 1997 from the pediatric hospital in Lisbon were bacteria in which antibiotic resistance was limited to β-lactam antibiotics. The other half were multidrug resistant. The coexistence of MRSA with such unequal antibiotic resistance profiles prompted us to use molecular typing techniques for the characterization of the MRSA strains. Fifty-three strains chosen randomly were typed by a combination of genotypic methods. Over 90% of the MRSA strains belonged to two clones: the most frequent one, designated the “pediatric clone,” was reminiscent of historically “early” MRSA: most isolates of this clone were only resistant to β-lactam antimicrobials and remained susceptible to macrolides, quinolones, clindamycin, spectinomycin, and tetracycline. They showed heterogeneous and low-level resistance to methicillin (MIC, 1.5 to 6 μg/ml), carried the ClaI-mecApolymorph II, were free of the transposon Tn554, and showed macrorestriction pattern D (clonal type II::NH::D). The second major clone was the internationally spread and multiresistant “Iberian” MRSA with homogeneous and high-level resistance to methicillin (MIC, >200 μg/ml) and clonal type I::E::A. Surprisingly, the multidrug-resistant and highly epidemic Iberian MRSA did not replace the much less resistant pediatric clone during the 6 years of surveillance. The pediatric clone was also identified among contemporary MRSA isolates from Poland, Argentina, The United States, and Colombia, and the overwhelming majority of these were also associated with pediatric settings. We propose that the pediatric MRSA strain represents a formerly widely spread archaic clone which survived in some epidemiological settings with relatively limited antimicrobial pressure.


1978 ◽  
Vol 81 (1) ◽  
pp. 131-138 ◽  
Author(s):  
W. A. Hawkins ◽  
J. W. Dale

SUMMARYThe results presented in this paper confirm the existence of two types of tetracycline resistance inShigella sonnei. One group of strains had a high level of resistance to tetracycline and oxytetracycline, with a variable level of minocycline resistance. The second group had a lower level of tetracycline resistance and were sensitive to minocycline. After conjugation withE. coliK12 the selectedE. colitransconjugants had the same levels of resistance as the parentSh. sonneistrain, with one exception.Sh. sonnei87 was resistant to a high level of tetracycline, but was able to transfer only low level resistance. It is suggested thatSh. sonnei87 carries two plasmids: pSU1, a conjugative plasmid conferring a low level of tetracycline resistance, and pSU2, a non-conjugative plasmid which confers a high level of resistance to tetracycline.


2019 ◽  
Vol 19 (28) ◽  
pp. 2554-2566 ◽  
Author(s):  
Aurelio Ortiz ◽  
Estibaliz Sansinenea

Background:: Candida species are in various parts of the human body as commensals. However, they can cause local mucosal infections and, sometimes, systemic infections in which Candida species can spread to all major organs and colonize them. Objective:: For the effective treatment of the mucosal infections and systemic life-threatening fungal diseases, a considerably large number of antifungal drugs have been developed and used for clinical purposes that comprise agents from four main drug classes: the polyenes, azoles, echinocandins, and antimetabolites. Method: : The synthesis of some of these drugs is available, allowing synthetic modification of the molecules to improve the biological activity against Candida species. The synthetic methodology for each compound is reviewed. Results: : The use of these compounds has caused a high-level resistance against these drugs, and therefore, new antifungal substances have been described in the last years. The organic synthesis of the known and new compounds is reported. Conclusion: : This article summarizes the chemistry of the existing agents, both the old drugs and new drugs, in the treatment of infections due to C. albicans, including the synthesis of the existing drugs.


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