PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “resistance evolution”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 613 records · Page 34Linked to original sources
PubMed2002

Evolution and spread of antibiotic resistance.

Antibiotic resistance is a clinical and socioeconomical problem that is here to stay. Resistance can be natural or acquired. Some bacterial species, such as Pseudomonas aeruginosa, show a high intrinsic resistance to a number of antibiotics whereas others are normally highly antibiotic susceptible such as group A streptococci. Acquired resistance evolve via genetic alterations in the microbes own genome or by horizontal transfer of resistance genes located on various types of mobile DNA elements. Mutation frequencies to resistance can vary dramatically depending on the mechanism of resistance and whether or not the organism exhibits a mutator phenotype. Resistance usually has a biological cost for the microorganism, but compensatory mutations accumulate rapidly that abolish this fitness cost, explaining why many types of resistances may never disappear in a bacterial population. Resistance frequently occurs stepwise making it important to identify organisms with low level resistance that otherwise may constitute the genetic platform for development of higher resistance levels. Self-replicating plasmids, prophages, transposons, integrons and resistance islands all represent DNA elements that frequently carry resistance genes into sensitive organisms. These elements add DNA to the microbe and utilize site-specific recombinases/integrases for their integration into the genome. However, resistance may also be created by homologous recombination events creating mosaic genes where each piece of the gene may come from a different microbe. The selection with antibiotics have informed us much about the various genetic mechanisms that are responsible for microbial evolution.

Animals↗
PubMed2001

Minimizing potential resistance: the molecular view.

The major contribution of molecular biology to the study of antibiotic resistance has been the elucidation of nearly all biochemical mechanisms of resistance and the routes for dissemination of genetic information among bacteria. In this review, we consider the potential contribution of molecular biology to counteracting the evolution of resistant bacteria. In particular, we emphasize the fact that fundamental approaches have had direct practical effects on minimizing potential resistance: by improving interpretation of resistance phenotypes, by providing more adequate human therapy, by fostering more prudent use of antibiotics, and by allowing the rational design of new drugs that evade existing resistance mechanisms or address unexploited targets.

Animals↗
PubMed1992

Fatal association between dieldrin-resistant and susceptible Australian sheep blowflies, Lucilia cuprina.

A novel phenomenon of interactions between genotypes of the dieldrin-resistance (Rdl) locus of the Australian sheep blowfly (Lucilia cuprina) is described. Susceptible adult flies exposed to dieldrin-resistant (Rdl/Rdl or Rdl/S) adults, raised from larvae grown on media containing sublethal concentrations of dieldrin, display mortality related to the concentration on which the resistant flies developed. The resistant flies excrete quantities of dieldrin that are toxic to susceptible flies. These observations provide an additional mechanism to those previously identified for the rapid evolution of resistance to dieldrin by L. cuprina.

Animals↗
PubMed1999

Integrative model for binding of Bacillus thuringiensis toxins in susceptible and resistant larvae of the diamondback moth (Plutella xylostella).

Insecticidal crystal proteins from Bacillus thuringiensis in sprays and transgenic crops are extremely useful for environmentally sound pest management, but their long-term efficacy is threatened by evolution of resistance by target pests. The diamondback moth (Plutella xylostella) is the first insect to evolve resistance to B. thuringiensis in open-field populations. The only known mechanism of resistance to B. thuringiensis in the diamondback moth is reduced binding of toxin to midgut binding sites. In the present work we analyzed competitive binding of B. thuringiensis toxins Cry1Aa, Cry1Ab, Cry1Ac, and Cry1F to brush border membrane vesicles from larval midguts in a susceptible strain and in resistant strains from the Philippines, Hawaii, and Pennsylvania. Based on the results, we propose a model for binding of B. thuringiensis crystal proteins in susceptible larvae with two binding sites for Cry1Aa, one of which is shared with Cry1Ab, Cry1Ac, and Cry1F. Our results show that the common binding site is altered in each of the three resistant strains. In the strain from the Philippines, the alteration reduced binding of Cry1Ab but did not affect binding of the other crystal proteins. In the resistant strains from Hawaii and Pennsylvania, the alteration affected binding of Cry1Aa, Cry1Ab, Cry1Ac, and Cry1F. Previously reported evidence that a single mutation can confer resistance to Cry1Ab, Cry1Ac, and Cry1F corresponds to expectations based on the binding model. However, the following two other observations do not: the mutation in the Philippines strain affected binding of only Cry1Ab, and one mutation was sufficient for resistance to Cry1Aa. The imperfect correspondence between the model and observations suggests that reduced binding is not the only mechanism of resistance in the diamondback moth and that some, but not all, patterns of resistance and cross-resistance can be predicted correctly from the results of competitive binding analyses of susceptible strains.

Animals↗
PubMed2005

Host microsatellite alleles in malaria predisposition?

BACKGROUND: Malaria is a serious, sometimes fatal, disease caused by Plasmodium infection of human red blood cells. The host-parasite co-evolutionary processes are well understood by the association of coding variations such as G6PD, Duffy blood group receptor, HLA, and beta-globin gene variants with malaria resistance. The profound genetic diversity in host is attributed to polymorphic microsatellites loci. The microsatellite alleles in bacterial species are known to have aided their survival in fatal environmental conditions. The fascinating question is whether microsatellites are genomic cushion in the human genome to combat disease stress and has cause-effect relationships with infections. PRESENTATION OF THE HYPOTHESIS: It is hypothesized that repeat units or alleles of microsatellites TH01 and D5S818, located in close proximity to beta-globin gene and immune regulatory region in human play a role in malaria predisposition. Association of alleles at aforesaid microsatellites with malaria infection was analysed. To overrule the false association in unrecognized population stratification, structure analysis and AMOVA were performed among the sampled groups. TESTING OF HYPOTHESIS: Associations of microsatellite alleles with malaria infection were verified using recombination rate, Chi-square, and powerful likelihood tests. Further investigation of population genetic structure, and AMOVA was done to rule out the confounding effects of population stratification in interpretation of association studies. IMPLICATION OF THE HYPOTHESIS: Lower recombination rate (theta) between microsatellites and genes implicated in host fitness; positive association between alleles-13 (D5S818), 9 (TH01) and strong susceptibility to Plasmodium falciparum; and alleles-12 (D5S818) and 6 (TH01) rendering resistance to human host were evident. The interesting fact emerging from the study was that while predisposition to malaria was a prehistoric attribute, among TH01 alleles; evolution of resistant allele-6 was a recent phenomenon, which could conceivably be driven by infection related selective forces. The host's microsatellite allelic associations with malaria infection were valid in the light of low genetic variance between sampled groups and no population stratification.

Alleles↗
PubMed2006

The biological cost of mutational antibiotic resistance: any practical conclusions?

A key parameter influencing the rate and trajectory of the evolution of antibiotic resistance is the fitness cost of resistance. Recent studies have demonstrated that antibiotic resistance, whether caused by target alteration or by other mechanisms, generally confers a reduction in fitness expressed as reduced growth, virulence or transmission. These findings imply that resistance might be reversible, provided antibiotic use is reduced. However, several processes act to stabilize resistance, including compensatory evolution where the fitness cost is ameliorated by additional mutation without loss of resistance, the rare occurrence of cost-free resistance mechanisms and genetic linkage or co-selection between the resistance markers and other selected markers. Conceivably we can use this knowledge to rationally choose and design targets and drugs where the costs of resistance are the highest, and where the likelihood of compensation is the lowest.

Adaptation, Physiological↗
PubMed2001

Anticancer drug resistance in primary human brain tumors.

The difficult clinical situation still associated with most types of primary human brain tumors has fostered significant interest in defining novel therapeutic modalities for this heterogeneous group of neoplasms. Beginning in the 1980s chemotherapy has been incorporated into the treatment protocol of a number of intractable brain tumors. However, it has predominantly failed to improve patient outcome. The unsatisfactory results with chemotherapeutic intervention have chiefly been attributed to tumor cell resistance. In recent years, there has been a literal explosion in our understanding about the mechanisms by which cancer cells become chemoresistant. During the course of their evolution (intrinsic resistance) or in response to chemotherapy (acquired resistance) these cells may follow a number of pathways of genetic alterations to possess a common (multidrug) or drug-specific (individual drug) resistant phenotype. Genomic aberrations, deregulation of membrane transporting proteins and cellular enzymes, and an altered susceptibility to commit to apoptosis are among the steps on the way that contribute to the genesis of chemotherapeutic treatment failure. Although, through the years we have come to yield information and inferences as to the roles that different molecular events may have in the resistance phenotype of cancer cells, the actual involvement of single genetic alterations in conferring drug resistance in primary brain tumors remains debatable. This uncertainty and, besides, the lack of proper drug resistance diagnostics, in a vicious circle, hinder the development of effective resistance-modulation strategies. Clinical non-responsiveness to chemotherapy remains a formidable obstacle to the successful treatment of brain tumors and one of the most serious problems to be solved in the therapy of these lesions. Future advances in the chemotherapeutic management of these neoplasms will come with an improved understanding of the significance and interrelationship of the multiple biological systems operative in promoting resistance to this treatment modality. The focus of this review is to summarize current knowledge concerning major drug resistance-related markers, to describe their functional interaction en route to chemoresistance, and to discuss their implication in rendering human brain tumor cells resistant to chemotherapy.

Animals↗
PubMed2006

Survey of antibiotic resistance in an integrated marine aquaculture system under oxolinic acid treatment.

The consequences of antibiotic use in aquatic integrated systems, which are based on trophic interactions between different cultured organisms and physical continuity through water, need to be examined. In this study, fish reared in a prototype marine integrated system were given an oxolinic acid treatment, during and after which the level of resistance to this quinolone antibiotic was monitored among vibrio populations from the digestive tracts of treated fish, co-cultured bivalves and sediments that were isolated on thiosulfate-citrate-bile-sucrose. Oxolinic acid minimum inhibitory concentration distributions obtained from replica plating of thiosulfate-citrate-bile-sucrose plates indicated that a selection towards oxolinic acid resistance had occurred in the intestines of fish under treatment. In contrast, and despite oxolinic acid concentrations higher than minimum inhibitory concentrations of susceptible bacteria, no clear evolution of resistance levels was detected either in bivalves or in sediments.

Animals↗
PubMed1993

Changing gravity level and the development of animals.

Space biology has accumulated a great body of information concerning the influence of microgravity upon objects of varying levels of biological organization: from microorganisms to higher animals and humans. However, the choice of biological objects was in most cases random, and there has been no attempt at a comparative biological analysis of the results obtained. A similar situation is noted in hypergravity research, where responses in various animal classes are compared mainly with respect to differences in body masses rather than in the level of biological organization. Without any claims to solve this serious problem in this presentation, I'll try to at least raise it, using as a starting point the conception about evolution of resistance and reactivity, created by my teacher N.N. Sirotinin (1981).

Acceleration↗
PubMed2000

Evolution of Streptococcus pneumoniae serotypes and antibiotic resistance in Belgium-update (1994-98).

OBJECTIVE: To follow the evolution of capsular types and resistance of Streptococcus pneumoniae, isolated from deep sites. METHODS: More than 100 Belgian laboratories permanently collect S. pneumoniae strains isolated from puncture specimens (blood, cerebrospinal fluid, middle ear fluid, etc.) and forward them to the reference center in Leuven, in order to determine the capsular serogroups and types (SGTs) and their resistance. RESULTS: From 1994 to 1998, the 5486 S. pneumoniae strains examined belonged to 39 of the 46 currently identified SGTs. The 10 most frequent SGTs accounted for 78.9% of the isolates, and 97% of all isolates belonged to SGTs included in the 23-valent vaccine. Overall mortality of patients with pneumococcal bacteremia or meningitis was 9.7%, and 23.8% in patients over 80 years. From 1994 to 1998, resistance to penicillin (P) increased from 7.6% to 14.2%, to tetracycline (T) from 14.9% to 28.0%, and to erythromycin (E) from 22.9% to 31%. Triple resistance (PTE) increased from 0.9% in 1994 to 6.6% in 1998. Five SGTs (6, 9, 14, 19 and 23) accounted for 50% of the isolates, but for > 90% of the penicillin-resistant or erythromycin-resistant isolates. CONCLUSIONS: Resistance of S. pneumoniae to penicillin, erythromycin and tetracycline is steadily increasing and is concentrated in five serotypes included in the 23-valent pneumococcal vaccine. Increasing resistance and high mortality of invasive infections are an incentive to vaccinate vulnerable groups.

Adolescent↗
PubMed1999

Antibiotic resistance versus small molecules, the chemical evolution.

Two discovery approaches directed to addressing the problem of increasing bacterial resistance are described. The first is a program to build activity against methicillin-resistant Staphylococcus aureus (MRSA) into the cephalosporin class of antibacterials, by enhancing affinity for PBP2a, the penicillin-binding protein responsible for this resistance. Through stepwise improvement in potency, human serum binding, solubility, and betalactamase stability, a stable of new compounds with excellent potential as anti-MRSA agents was realized. From this set was chosen MC-02, 479 (RWJ-54428), which is now undergoing extensive preclinical evaluation. The second approach explores the uridyl peptide family of antibiotics, inhibitors of bacterial translocase (mraY), whose members include the pacidamycins, mureidomycins, and napsamycins. Access to a diverse set of analogs by total synthesis was catalyzed by the discovery that hydrogenation of the 4'-exoenamidofuranosyl moiety causes no loss in biological activity. Indepth exploration of SAR required (1) establishment of the absolute stereochemistry of the central diaminobutyric acid (DABA) moiety and (2) determination of the stereochemistry of the 4'-substituent on the deoxyfuranose unit. The former was accomplished by comparison of DABA derived from degradation of a natural product pacidamycin with a sample synthesized from L-threonine. The biological activity of one member of a synthesized library of possible stereoisomers of the natural product established the absolute stereochemistry of the remaining centers. A variety of analogs of the natural product were prepared utilizing the synthetic methods developed, and their biological activities provide important insights into the specificity and spectrum of the antibiotic class.

Animals↗
PubMed2002

Frequency of alleles conferring resistance to Bt maize in French and US corn belt populations of the European corn borer, Ostrinia nubilalis.

Farmers, industry, governments and environmental groups agree that it would be useful to manage transgenic crops producing insecticidal proteins to delay the evolution of resistance in target pests. The main strategy proposed for delaying resistance to Bacillus thuringiensis ( Bt) toxins in transgenic crops is the high-dose/refuge strategy. This strategy is based on the unverified assumption that resistance alleles are initially rare (<10(-3)). We used an F(2) screen on >1,200 isofemale lines of Ostrinia nubilalis Hübner (Lepidoptera: Crambidae) collected in France and the US corn belt during 1999-2001. In none of the isofemale lines did we detect alleles conferring resistance to Bt maize producing the Cry1Ab toxin. A Bayesian analysis of the data indicates that the frequency of resistance alleles in France was <9.20 x 10(-4) with 95% probability, and a detection probability of >80%. In the northern US corn belt, the frequency of resistance to Bt maize was <4.23 x 10(-4) with 95% probability, and a detection probability of >90%. Only 95 lines have been screened from the southern US corn belt, so these data are still inconclusive. These results suggest that resistance is probably rare enough in France and the northern US corn belt for the high-dose plus refuge strategy to delay resistance to Bt maize.

Alleles↗
PubMed2002

Analysis of the sequence and expression of a second putative acetylcholinesterase cDNA from organophosphate-susceptible and organophosphate-resistant cattle ticks.

The cattle tick, Boophilus microplus, is a major pest of cattle in Australia, Central and South America, and parts of Africa and Asia. Control of ticks with organophosphates (OPs) and carbamates, which target acetylcholinesterases (AChE), led to evolution of resistance to these pesticides. Alleles at the locus studied here, AChE2, from OP-susceptible female ticks from Australia and Mexico differed at 46 of 1689 nucleotide positions (20 putative amino acid differences) whereas alleles from three strains of OP-resistant ticks from Australia differed with the allele from the Australian susceptible ticks at six to 13 nucleotide positions (three to six putative amino acid differences). However, the role, if any, of these polymorphisms in the OP-resistance phenotype is unknown. Certainly none of the polymorphisms correspond to sites in AChE that are involved in catalysis or binding of acetylcholine in other organisms. Both of the AChE loci of B. microplus, AChE1 and AChE2, are apparently expressed in synganglia; AChE1 is also expressed in salivary glands and ovaries, in OP-susceptible and OP-resistant ticks. This seems to contradict studies of enzyme kinetics, which indicated that only one form of AChE was present in the synganglia, the site of the action of OPs, in this species of tick.

Acetylcholinesterase↗
PubMed2001

The development of bifenthrin resistance in two-spotted spider mite (Acari: Tetranychidae) from Australian cotton.

Bifenthrin (Talstar) was registered at the beginning of the 1993/94 season for control of Helicoverpa spp. and Tetranychus urticae in Australian cotton. Resistance was monitored in T. urticae following registration but despite the implementation of resistance management, resistance evolved in the 1996/97 cotton-growing season after only four seasons use. During the following three seasons resistance increased progressively both in level (from 1.2- to 109-fold at LC50) and abundance (from 20 to 90% strains) and was linked to field control failures. The evolution of resistance has now reduced the reliability of bifenthrin for T. urticae control in Australian cotton. The impact of bifenthrin resistance in T urticae and its continued management in Australian cotton is discussed.

Animals↗
PubMed2005

Using a generational time-step model to simulate dynamics of adaptation to transgenic corn and crop rotation by western corn rootworm (Coleoptera: Chrysomelidae).

We expanded a simulation model of the population dynamics and genetics of the western corn rootworm for a landscape of corn, soybean, and other crops to study the simultaneous development of resistance to both crop rotation and transgenic corn. Transgenic corn effective against corn rootworm was recently approved in 2003 and may be a very effective new technology for control of western corn rootworm in areas with or without the rotation-resistant variant. In simulations of areas with rotation-resistant populations, planting transgenic corn to only rotated cornfields was a robust strategy to prevent resistance to both traits. In these areas, planting transgenic corn to only continuous fields was not an effective strategy for preventing adaptation to crop rotation or transgenic corn. In areas without rotation-resistant phenotypes, gene expression of the allele for resistance to transgenic corn was the most important factor affecting the development of resistance to transgenic corn. If the allele for resistance to transgenic corn is recessive, resistance can be delayed longer than 15 yr, but if the resistant allele is dominant then resistance usually developed within 15 yr. In a sensitivity analysis, among the parameters investigated, initial allele frequency and density dependence were the two most important factors affecting the evolution of resistance. We compared the results of this simulation model with a more complicated model and results between the two were similar. This indicates that results from a simpler model with a generational time-step can compare favorably with a more complex model with a daily time-step.

Adaptation, Physiological↗
PubMed1982

Multiply antibiotic-resistant Staphylococcus aureus: introduction, transmission, and evolution of nosocomial infection.

A burn patient with a multiply antibiotic-resistant Staphylococcus aureus infection was transferred to Harborview Medical Center from a burn unit in another state. Despite standard wound precautions, transmission to 34 patients occurred during the subsequent 15 months. Twenty-seven of the patients were infected. Disease included pneumonia, empyema, bacteremia, endocarditis, osteomyelitis, and burn and wound infections. Seventeen of the 34 patients died. Phage typing and plasmid analysis showed the spread of multiply resistant S. aureus from the burn unit to the surgical intensive care unit where a study evaluating the use of chloramphenicol in cases of bowel sepsis was in progress. During this period the organism became resistant to chloramphenicol by acquiring either of two chloramphenicol R-plasmids. Using plasmid profiles and antibiograms, four epidemic strains were identified that assisted in identifying patient and personnel reservoirs. The outbreak was controlled only after rifampin was added to vancomycin treatment of infected patients, which correlated with eradication of the carrier state.

Adult↗