scholarly journals Resistance to vancomycin and teicoplanin: an emerging clinical problem.

1990 ◽  
Vol 3 (3) ◽  
pp. 280-291 ◽  
Author(s):  
A P Johnson ◽  
A H Uttley ◽  
N Woodford ◽  
R C George
Keyword(s):  
Clinical Problem ◽  
Selective Advantage ◽  
Vancomycin Resistance ◽  
Cross Resistance ◽  
Resistant Bacteria ◽  
Coagulase Negative Staphylococci ◽  
Wide Range ◽  
Vancomycin Mics ◽  
High Level ◽  
Level Resistance

Vancomycin and teicoplanin are glycopeptides active against a wide range of gram-positive bacteria. For 30 years following the discovery of vancomycin in 1956, vancomycin resistance was not detected among normally susceptible bacteria recovered from human specimens. Since 1986, however, bacteria resistant to vancomycin or teicoplanin or both have been described. Strains of the genera Leuconostoc, Lactobacillus, Pediococcus, and Erysipelothrix seem inherently resistant to glycopeptides. Species and strains of enterococci and coagulase-negative staphylococci appear to have acquired or developed resistance. There are at least two categories of glycopeptide resistance among enterococci, characterized by either high-level resistance to vancomycin (MIC, greater than or equal to 64 mg/liter) and teicoplanin (MIC, greater than or equal to 8 mg/liter) or lower-level vancomycin resistance (MIC, 32 to 64 mg/liter) and teicoplanin susceptibility (MIC, less than or equal to 1 mg/liter). The two categories appear to have similar resistance mechanisms, although genetic and biochemical studies indicate that they have arisen independently. Among coagulase-negative staphylococci, strains for which vancomycin MICs are up to 20 mg/liter or teicoplanin MICs are 16 to 32 mg/liter have been reported, but cross-resistance between these glycopeptides varies. The selective advantage accorded to glycopeptide-resistant bacteria and the observation that high-level resistance in enterococci is transferable suggest that such resistance may be expected to increase in incidence. Clinicians and microbiologists need to be aware of this emerging problem.

scholarly journals Biochemical and molecular characterization of Alternaria alternata isolates highly resistant to procymidone from broccoli and cabbage

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Bingran Wang ◽  
Tiancheng Lou ◽  
Lingling Wei ◽  
Wenchan Chen ◽  
Longbing Huang ◽  
...  
Keyword(s):  
Alternaria Alternata ◽  
Single Point ◽  
Sodium Dodecyl ◽  
Cross Resistance ◽  
Molecular Characteristics ◽  
Single Point Mutation ◽  
Wide Range ◽  
Significant Difference ◽  
Leaf Blights ◽  
High Level

AbstractAlternaria alternata, a causal agent of leaf blights and spots on a wide range of hosts, has a high risk of developing resistance to fungicides. Procymidone, a dicarboximide fungicide (DCF), has been widely used in controlling Alternaria leaf blights in China for decades. However, the resistance of A. alternata against DCFs has rarely been reported from crucifer plants. A total of 198 A. alternata isolates were collected from commercial fields of broccoli and cabbage during 2018–2019, and their sensitivities to procymidone were determined. Biochemical and molecular characteristics were subsequently compared between the high-level procymidone-resistant (ProHR) and procymidone-sensitive (ProS) isolates, and also between ProHR isolates from broccoli and cabbage. Compared with ProS isolates, the mycelial growth rate, sporulation capacity and virulence of most ProHR isolates were reduced; ProHR isolates displayed an increased sensitivity to osmotic stresses and a reduced sensitivity to sodium dodecyl sulfate (SDS); all ProHR isolates showed a reduced sensitivity to hydrogen peroxide (H2O2) except for the isolate B102. Correlation analysis revealed a positive cross-resistance between procymidone and iprodione, or fludioxonil. When treated with 10 μg/mL of procymidone, both mycelial intracellular glycerol accumulations (MIGAs) and relative expression of AaHK1 in ProS isolates were higher than those in ProHR isolates. Sequence alignment of AaHK1 from ten ProHR isolates demonstrated that five of them possessed a single-point mutation (P94A, V612L, E708K or Q924STOP), and four isolates had an insertion or a deletion in their coding regions. No significant difference in biochemical characteristics was observed among ProHR isolates from two different hosts, though mutations in AaHK1 of the cabbage-originated ProHR isolates were distinct from those of the broccoli-originated ProHR isolates.

scholarly journals Outbreak of Mupirocin-Resistant Staphylococci in a Hospital in Warsaw, Poland, Due to Plasmid Transmission and Clonal Spread of Several Strains

1999 ◽  
Vol 37 (9) ◽  
pp. 2781-2788 ◽  
Author(s):  
Tomasz A. Łe˛ski ◽  
Marek Gniadkowski ◽  
Anna Skoczyńska ◽  
Elz˙bieta Stefaniuk ◽  
Krzysztof Trzciński ◽  
...  
Keyword(s):  
Resistance Mechanisms ◽  
Hospital Environment ◽  
Coagulase Negative Staphylococci ◽  
Large Hospital ◽  
Methicillin Resistant ◽  
Inappropriate Use ◽  
Clonal Spread ◽  
High Level ◽  
Almost All ◽  
Level Resistance

An outbreak of mupirocin-resistant (MuR) staphylococci was investigated in two wards of a large hospital in Warsaw, Poland. Fifty-three MuR isolates of Staphylococcus aureus, S. epidermidis, S. haemolyticus, S. xylosus, and S. capitis were identified over a 17-month survey which was carried out after introduction of the drug for the treatment of skin infections. The isolates were collected from patients with infections, environmental samples, and carriers; they constituted 19.5% of all staphylococcal isolates identified in the two wards during that time. Almost all the MuR isolates were also resistant to methicillin (methicillin-resistant S. aureus and methicillin-resistant coagulase-negative staphylococci). Seven of the outbreak isolates expressed a low-level-resistance phenotype (MuL), whereas the remaining majority of isolates were found to be highly resistant to mupirocin (MuH). The mupA gene, responsible for the MuH phenotype, has been assigned to three different polymorphic loci among the strains in the collection analyzed. The predominant polymorph, polymorph I (characterized by a mupA-containingEcoRI DNA fragment of about 16 kb), was located on a specific plasmid which was widely distributed among the entire staphylococcal population. All MuR S. aureus isolates were found to represent a single epidemic strain, which was clonally disseminated in both wards. The S. epidermidis population was much more diverse; however, at least four clusters of closely related isolates were identified, which suggested that some strains of this species were also clonally spread in the hospital environment. Six isolates of S. epidermidis were demonstrated to express the MuL and MuH resistance mechanisms simultaneously, and this is the first identification of such dual MuR phenotype-bearing strains. The outbreak was attributed to a high level and inappropriate use of mupirocin, and as a result the dermatological formulation of the drug has been removed from the hospital formulary.

scholarly journals Antimicrobial Resistance of DiarrheagenicEscherichia coli Isolated from Children under the Age of 5 Years from Ifakara, Tanzania

1999 ◽  
Vol 43 (12) ◽  
pp. 3022-3024 ◽  
Author(s):  
Jordi Vila ◽  
Martha Vargas ◽  
Climent Casals ◽  
Honorato Urassa ◽  
Hassan Mshinda ◽  
...  
Keyword(s):  
Developing Countries ◽  
Public Health Problem ◽  
Multidrug Resistant ◽  
Resistant Bacteria ◽  
Important Public Health Problem ◽  
Important Public Health ◽  
E Coli ◽  
High Level ◽  
Level Resistance ◽  
Children Under 5

ABSTRACT Diarrhea caused by multidrug-resistant bacteria is an important public health problem among children in developing countries. The prevalence and antimicrobial susceptibility of diarrheagenicEscherichia coli in 346 children under 5 years of age in Ifakara, Tanzania, were studied. Thirty-eight percent of the cases of diarrhea were due to multiresistant enterotoxigenic E. coli, enteroaggregative E. coli, or enteropathogenicE. coli. Strains of all three E. colicategories showed high-level resistance to ampicillin, tetracycline, co-trimoxazole, and chloramphenicol but were highly susceptible to quinolones. Guidelines for appropriate use of antibiotics in developing countries need updating.

scholarly journals Selection of High-Level Resistance to Human Immunodeficiency Virus Type 1 Protease Inhibitors

2003 ◽  
Vol 47 (2) ◽  
pp. 759-769 ◽  
Author(s):  
Terri Watkins ◽  
Wolfgang Resch ◽  
David Irlbeck ◽  
Ronald Swanstrom
Keyword(s):  
Human Immunodeficiency Virus ◽  
Protease Inhibitors ◽  
Human Immunodeficiency Virus Type ◽  
Selective Pressure ◽  
Cross Resistance ◽  
Resistance Mutations ◽  
Immunodeficiency Virus ◽  
High Level ◽  
Level Resistance

ABSTRACT Protease inhibitors represent some of the most potent agents available for therapeutic strategies designed to inhibit human immunodeficiency virus type 1 (HIV-1) replication. Under certain circumstances the virus develops resistance to the inhibitor, thereby negating the benefits of this therapy. We have carried out selections for high-level resistance to each of three protease inhibitors (indinavir, ritonavir, and saquinavir) in cell culture. Mutations accumulated over most of the course of the increasing selective pressure. There was significant overlap in the identity of the mutations selected with the different inhibitors, and this gave rise to high levels of cross-resistance. Virus particles from the resistant variants all showed defects in processing at the NC/p1 protease cleavage site in Gag. Selections with pairs of inhibitors yielded similar patterns of resistance mutations. A virus that could replicate at near-toxic levels of the three protease inhibitors combined was selected. The pro sequence of this virus was similar to that of the viruses that had been selected for high-level resistance to each of the drugs singly. Finally, a molecular clone carrying the eight most common resistance mutations seen in these selections was characterized. The sequence of this virus was relatively stable during selection for revertants in spite of displaying poor processing at the NC/p1 site and having significantly reduced fitness. These results reveal patterns of drug resistance that extend to near the limits of attainable selective pressure with these inhibitors and confirm the patterns of cross-resistance for these three inhibitors and the attenuation of virion protein processing and fitness that accompanies high-level resistance.

scholarly journals High-level vancomycin-resistant enterococci causing hospital infections

1989 ◽  
Vol 103 (1) ◽  
pp. 173-181 ◽  
Author(s):  
A. H. C. Uttley ◽  
R. C. George ◽  
J. Naidoo ◽  
N. Woodford ◽  
A. P. Johnson ◽  
...  
Keyword(s):  
Plasmid Dna ◽  
Vancomycin Resistance ◽  
Recipient Strain ◽  
Hospital Infections ◽  
Minimal Inhibitory Concentrations ◽  
Vancomycin Resistant Enterococci ◽  
Vancomycin Resistant ◽  
Many Sources ◽  
High Level ◽  
Level Resistance

SUMMARYNosocomial infection or colonization due to enterococci with high-level resistance to vancomycin (minimal inhibitory concentrations [MICs] between 64 and > 2000 mg/L) has occurred in 41 patients with renal disease. These vancomycin-resistant enterococci were cultured from many sources including blood. All but one strain contained one or more plasmids ranging in molecular weight from 1·0 to 40 Megadaltons (MDa). Vancomycin resistance was transferable by conjugation to a susceptible recipient strain ofEnterococcus faecalisbut this was not always associated with plasmid DNA. The emergence of transferable high-level vancomycin resistance in enterococci causing significant clinical infections is of particular importance since vancomycin is widely regarded as a reserve drug for the management of infections with multi-resistant Gram-positive organisms.

scholarly journals High-Level Pacidamycin Resistance in Pseudomonas aeruginosa Is Mediated by an Opp Oligopeptide Permease Encoded by theopp-fabIOperon

2013 ◽  
Vol 57 (11) ◽  
pp. 5565-5571 ◽  
Author(s):  
Anita Mistry ◽  
Mark S. Warren ◽  
John K. Cusick ◽  
RoxAnn R. Karkhoff-Schweizer ◽  
Olga Lomovskaya ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
High Frequency ◽  
Cross Resistance ◽  
Peptide Antibiotics ◽  
Content Type ◽  
Resistant Mutants ◽  
High Level ◽  
Level Resistance ◽  
Resistance Mutants

ABSTRACTPacidamycins (or uridyl peptide antibiotics) possess selectivein vivoactivity againstPseudomonas aeruginosa. An important limitation for the therapeutic use of pacidamycins withP. aeruginosais the high frequency (10−6to 10−7) at which resistant mutants emerge. To elucidate the mechanism(s) of this resistance, pacidamycin-resistantP. aeruginosamutants were isolated. Two types of mutants were obtained. Type 1, or high-level resistance mutants with a pacidamycin MIC of 512 μg/ml, were more abundant, with a frequency of ∼2 × 10−6, and did not show cross-resistance with other antibiotics. Type 2, low-level resistance mutants, were isolated with a frequency of ∼10−8and had a pacidamycin MIC of 64 μg/ml (the MIC for the wild-type strain was 4 to 16 μg/ml). These mutants were cross-resistant to levofloxacin, tetracycline, and erythromycin and were shown to overexpress either the MexAB-OprM or MexCD-OprJ multidrug resistance efflux pumps. High-level resistant mutants were isolated by transposon mutagenesis and one insertion was localized tooppB, one of two periplasmic binding protein components of an oligopeptide transport system which is encoded by theopp-fabIoperon. The Opp system is required for uptake of pacidamycin across the inner membrane, since variousopp, but notfabI, mutants were resistant to high levels of pacidamycin. Both of the two putative Opp periplasmic binding proteins, OppA and OppB, were required for pacidamycin uptake. Although both impaired uptake into and efflux from the cell can cause pacidamycin resistance inP. aeruginosa, our data suggest that impaired uptake is the primary reason for the high-frequency and high-level pacidamycin resistance.

scholarly journals Failure of VITEK2 to reliably detect vanB- mediated vancomycin resistance in Enterococcus faecium

2020 ◽  
Author(s):  
Sarah V. Walker ◽  
Martina Wolke ◽  
Georg Plum ◽  
Robert E. Weber ◽  
Guido Werner ◽  
...  
Keyword(s):  
Enterococcus Faecium ◽  
Vancomycin Resistance ◽  
Bacterial Suspension ◽  
Initial Growth ◽  
Low Level ◽  
Test Kit ◽  
Before And After ◽  
Vancomycin Resistant ◽  
High Level ◽  
Level Resistance

AbstractObjectivesThe increasing prevalence of vancomycin resistant enterococci (VRE) necessitates a reliable detection of VRE especially for low level resistance mediated by vanB in Enterococcus faecium. In this prospective study we analyzed if vanB mediated vancomycin resistance can be reliably detected by Vitek2.Methods1344 enterococcal isolates from routine clinical specimens were tested by Vitek2 (bioMérieux, Nürtingen, Germany). Additionally, a bacterial suspension (0.5 McFarland) was inoculated on a chromID VRE screening agar (bioMérieux) and incubated for 48 hours. If vancomycin was tested susceptible by Vitek2 but growth was detected on the screening agar a PCR for vanA/vanB was performed (GeneXpert vanA/B test kit, Cepheid, Frankfurt, Germany). MICs of vancomycin susceptible by Vitek but vanA/B positive isolates were determined before and after cultivation in a broth with increasing concentration of vancomycin.Results156/492 of E. faecium were VRE, predominantly vanB (87.0%) of which 14 were not identified as VRE by Vitek2 (sensitivity 91.0%). The majority (9/14) demonstrated high-level MICs by broth dilution. Even after exposure to increasing vancomycin concentrations MICs remained nearly identical. Three of the undetected isolates demonstrated initial growth on chromID VRE, after the vancomycin exposure additional 7 isolates demonstrated growth on chromID VRE.ConclusionsVitek2 fails to detect vanB mediated vancomycin resistance consistently, especially but not limited to low-level resistance. As this may lead to treatment failure and further dissemination of vanB VRE, additional methods (e.g. culture on VRE screening agar or PCR) are necessary to reliably identify vanB-positive enterococci in clinical routine.

scholarly journals Contribution of rpoB Mutations to Development of Rifamycin Cross-Resistance in Mycobacterium tuberculosis

1998 ◽  
Vol 42 (7) ◽  
pp. 1853-1857 ◽  
Author(s):  
D. L. Williams ◽  
L. Spring ◽  
L. Collins ◽  
L. P. Miller ◽  
L. B. Heifets ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Cross Resistance ◽  
In Vitro Mutagenesis ◽  
Missense Mutations ◽  
Resistance Mutations ◽  
Development Of Resistance ◽  
High Level ◽  
The Impact ◽  
Level Resistance

ABSTRACT The contributions of 23 insertion, deletion, or missense mutations within an 81-bp fragment of rpoB, the gene encoding the β-subunit of the DNA-dependent RNA polymerase of Mycobacterium tuberculosis, to the development of resistance to rifamycins (rifampin, rifabutin, rifapentine, and KRM-1648) in 29 rifampin-resistant clinical isolates were defined. Specific mutantrpoB alleles led to the development of cross-resistance to all rifamycins tested, while a subset of mutations were associated with resistance to rifampin and rifapentine but not to KRM-1648 or rifabutin. To further study the impact of specific rpoBmutant alleles on the development of rifamycin resistance, mutations were incorporated into the rpoB gene of M. tuberculosis H37Rv, contained on a mycobacterial shuttle plasmid, by in vitro mutagenesis. Recombinant M. tuberculosis clones containing plasmids with specific mutations in either codon 531 or 526 of rpoB exhibited high-level resistance to all rifamycins tested, whereas clones containing a plasmid with a mutation in codon 516 exhibited high-level resistance to rifampin and rifapentine but were susceptible to both rifabutin and KRM-1648. These results provided additional proof of the association of specificrpoB mutations with the development of rifamycin resistance and corroborate previous reports of the usefulness of rpoB genotyping for predicting rifamycin-resistant phenotypes.

scholarly journals Characterization of an Enterococcus gallinarum Isolate Carrying a DualvanAandvanBCassette

2015 ◽  
Vol 53 (7) ◽  
pp. 2225-2229 ◽  
Author(s):  
Alireza Eshaghi ◽  
Dea Shahinas ◽  
Aimin Li ◽  
Ruwandi Kariyawasam ◽  
Philip Banh ◽  
...  
Keyword(s):  
Clinical Isolate ◽  
Resistance Mechanism ◽  
Vancomycin Resistance ◽  
Content Type ◽  
Enterococcal Species ◽  
Enterococcus Gallinarum ◽  
High Level ◽  
Identification And Characterization ◽  
Level Resistance

The ability of vancomycin resistance determinants to be horizontally transferred within enterococci species is a concern. Identification and characterization of vancomycin-resistant enterococci (VRE) in a clinical isolate have a significant impact on infection control practices. In this study, we describe a clinical isolate ofEnterococcus gallinarumexhibiting high-level resistance to vancomycin and teicoplanin. The genetic characterization of this isolate showed the presence ofvanAandvanBgenes in addition to the naturally carriedvanCgene.vanAwas identified on pA6981, a 35,608-bp circular plasmid with significant homology to plasmid pS177. ThevanBoperon was integrated into the bacterial chromosome and showed a high level of homology to previously reported Tn1549and Tn5382. To the best of our knowledge, this is the first report ofE. gallinarumcarrying bothvanAandvanBoperons, indicating the importance of identifying the vancomycin resistance mechanism in non-E. faeciumand non-E. faecalisenterococcal species.

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