[Evolution of acquired drug resistance of Mycobacterium tuberculosis. Studies made in the period 1963-1965 at the Clinica Tisiologica of the University of Milan].
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Antitubercular Agents↗
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Results for “resistance evolution”
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Effect of glucan on murine lupus evolution and on host resistance to Klebsiella pneumoniae.
Glucan is a polysaccharide from the yeast Saccharomyces cerevisiae that stimulates the mononuclear phagocytic system (MPS). NZB/NZW F1 mice were divided into two groups: one group received a subcutaneous injection of 0.5 mg glucan/animal for 1 week, and the other received the same dose for 3 months. No changes were observed in those animals submitted to short-term glucan treatment, whereas animals with active lupus and submitted to long-term glucan administration presented early death, with significant differences in accumulated mortality rates over 33-37 weeks, when compared to controls. No deaths were observed in lupus mice treated with glucan 24 hours before the induction of septic shock by Klebsiella pneumoniae, in contrast to mortality of 95.3% in the control group during the follow-up period of 12 days. We conclude that although glucan is able to exacerbate lupus activity, it enhances resistance to infection in lupus mice.
Animals↗
Isolation of tetracycline-resistant Megasphaera elsdenii strains with novel mosaic gene combinations of tet(O) and tet(W) from swine.
Anaerobic bacteria insensitive to chlortetracycline (64 to 256 microg/ml) were isolated from cecal contents and cecal tissues of swine fed or not fed chlortetracycline. A nutritionally complex, rumen fluid-based medium was used for culturing the bacteria. Eight of 84 isolates from seven different animals were identified as Megasphaera elsdenii strains based on their large-coccus morphology, rapid growth on lactate, and 16S ribosomal DNA sequence similarities with M. elsdenii LC-1(T). All eight strains had tetracycline MICs of between 128 and 256 microg/ml. Based on PCR assays differentiating 14 tet classes, the strains gave a positive reaction for the tet(O) gene. By contrast, three ruminant M. elsdenii strains recovered from 30-year-old culture stocks had tetracycline MICs of 4 microg/ml and did not contain tet genes. The tet genes of two tetracycline-resistant M. elsdenii strains were amplified and cloned. Both genes bestowed tetracycline resistance (MIC = 32 to 64 microg/ml) on recombinant Escherichia coli strains. Sequence analysis revealed that the M. elsdenii genes represent two different mosaic genes formed by interclass (double-crossover) recombination events involving tet(O) and tet(W). One or the other genotype was present in each of the eight tetracycline-resistant M. elsdenii strains isolated in these studies. These findings suggest a role for commensal bacteria not only in the preservation and dissemination of antibiotic resistance in the intestinal tract but also in the evolution of resistance.
Animals↗
Evolution of high-level, multiple anthelmintic resistance on a sheep farm in Malaysia.
Anthelmintic resistance in nematode parasites of sheep and goats on a government farm in north Malaysia was monitored over a 3-year period (1997-2000). The faecal egg count reduction test (FECRT) was conducted on young sheep at the beginning and end of this period. Changes in management, designed to reduce the selection pressure for the development of anthelmintic resistance, were also implemented during this time. By far the most important parasite problem was Haemonchus contortus. In 1997, this nematode was found to be resistant to levamisole, with suspected resistance to closantel and moxidectin. However, when the FECRT was repeated 3 years later, its resistance status had become much more severe, with resistance to benzimidazole, levamisole and ivermectin, and suspected resistance to moxidectin. This rapid evolution to multiple anthelmintic resistance is a major concern that needs to be arrested. There is an urgent need to evaluate other control strategies that incorporate livestock management, the 'smart' use of drugs and non-chemotherapeutic approaches, such as biological control agents.
Animals↗
Antibiotic exposure as a risk factor for emergence of resistance: the influence of concentration.
Evolution of antibiotic resistance (AR) is increasingly perceived as a major clinical problem. The use of bactericidal antibiotics may protect against this, to some extent, by eradication of the pathogen, but the borders between cidal and inhibitory activity in the patient are often blurred. In addition, there are clinical reasons why eradication of the pathogen may not always be desirable. Antibiotic dosing schedules are currently driven by the perception that T >MIC and AUIC are the main predictors of outcome for time-dependent and concentration-dependent antibiotics, respectively. In the context of protecting against development of resistance in the pathogen however, peak antibiotic concentration and the concept of mutant prevention concentrations may be more important. The role of post-antibiotic and sub-MIC effects is more conjectural. Considerations of mechanisms of resistance and their relationship to antibiotic dosing schedules will also be highlighted. Lastly, the relevance of all this to the development of resistance in the normal bacterial flora will be discussed.
Anti-Bacterial Agents↗
Antibiotic exposure as a risk factor for emergence of resistance: the influence of concentration.
Evolution of antibiotic resistance (AR) is increasingly perceived as a major clinical problem. The use of bactericidal antibiotics may protect against this, to some extent, by eradication of the pathogen, but the borders between cidal and inhibitory activity in the patient are often blurred. In addition, there are clinical reasons why eradication of the pathogen may not always be desirable. Antibiotic dosing schedules are currently driven by the perception that T > MIC and AUIC are the main predictors of outcome for time-dependent and concentration-dependent antibiotics, respectively. In the context of protecting against development of resistance in the pathogen however, peak antibiotic concentration and the concept of mutant prevention concentrations may be more important. The role of post-antibiotic and sub-MIC effects is more conjectural. Considerations of mechanisms of resistance and their relationship to antibiotic dosing schedules will also be highlighted. Lastly, the relevance of all this to the development of resistance in the normal bacterial flora will be discussed.
Anti-Bacterial Agents↗
[Development of resistance to aminoglycosides in hospital strains of Serratia].
A study on the evolution of resistance to six aminoglycosides in Serratia as well as the relationship with the annual consumption of each drug in a hospital over the period 1974-1981 was carried out. The incidence of modifying enzymes and their genetical location was determined in 38 isolates. It was found that: The variations in the percentage of Sm clinical isolates showed no relationship with the consumption of Sm. Two different types of enzymes are involved in this resistance: AAD(3''): adenylyltransferase and APH(3''): phosphotransferase. The resistance to Nm, Km and Gm seems to be directly related with the continuous consumption of these drugs. In all the strains under study (Nm-Km)r was due to an APH(3')(5)I: phosphotransferase, Gmr to two types of acetyltransferases: AAC(3)I, only found in strains isolated before 1977 and AAC(3)II which predominates in 1981. After introducing Tm (1975) and Ak (1979) in our environment, there was an increase in the number of resistant strains. Two acetyltransferases with Tm-affinity were found: AAC(3)II and AAC(6')IV, the latter showing affinity for AKr. It was determined that five of these enzymes are plasmid-mediated. The genetical location of a sixth enzyme (AAC(6')IV) has not been clarified.
Acetyltransferases↗
Modelling parasite drug resistance: lessons for management and control strategies.
Mathematical models of the evolution of drug resistance in infectious diseases are predominantly concentrated in three main areas: antimalarial, antibiotic and anthelmintic resistance. There appears to be little or no cross-reference between them. This literature was examined to identify factors that influence the evolution of drug resistance irrespective of the species and drug under study. The aim is to provide non-technical readers with a basic qualitative understanding of the issues and pitfalls involved in designing drug treatment regimens to minimize the evolution of resistance. The principal factors determining the rate at which resistance evolves appear to be (i) the starting frequency of resistance, (ii) the level and pattern of drug use, (iii) the drug's pharmacokinetic properties, (iv) the number of genes required to encode resistance, (v) the level of sexual recombination in the parasite population, (vi) intrahost dynamics and, in particular, whether 'crowding' effects are present, (vii) the genetic basis of resistance and (viii) the number of individual parasites in an infection. The relative importance of these factors depends on the biology of the organisms under consideration and external factors such as the extent to which the infrastructure of health care delivery constrains the practicalities of drug regimens.
Animals↗
Evolution of antifungal-drug resistance: mechanisms and pathogen fitness.
Like other microorganisms, fungi exist in populations that are adaptable. Under the selection imposed by antifungal drugs, drug-sensitive fungal pathogens frequently evolve resistance. Although the molecular mechanisms of resistance are well-characterized, there are few measurements of the impact of these mechanisms on pathogen fitness in different environments. To predict resistance before a new drug is prescribed in the clinic, the full spectrum of potential resistance mutations and the interactions among combinations of divergent mechanisms can be determined in evolution experiments. In the search for new strategies to manage drug resistance, measuring the limits of adaptation might reveal methods for trapping fungal pathogens in evolutionary dead ends.
Antifungal Agents↗
[Aminoglycoside 3'-phosphotransferase genes: a model of the evolution of determinants of the resistance to aminoglycoside antibiotics].
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Aminoglycosides↗
Bi-trophic mathematical model for pest adaptation to a resistant crop.
A version of the Lotka-Volterra predator-prey model with logistic crop growth is modified to explore the rate of adaptation of a herbivore to a pest-resistant crop. This provides a phenotypic model for the evolution of resistance in a population comprising three different pest types each defined by differing parameter values for respiration rate and crop palatability. Expressions estimating the rates of increase of the fitter pest types are obtained as a function of the food qualities, and respiration and mortality rates. Potential strategies for delaying the rate of adaptation with regard to the expressions derived above, via the use of pest-susceptible refugia and natural enemies, are discussed. Although the model is formulated as one in which a single gene is the factor conferring resistance it can be interpreted and used independently of this.
Adaptation, Physiological↗
Fluoroquinolone resistance of Escherichia coli at a cancer center: epidemiologic evolution and effects of discontinuing prophylactic fluoroquinolone use in neutropenic patients with leukemia.
The aim of the present study was to investigate the epidemiologic evolution of fluoroquinolone resistance of E. coli clinical isolates from patients admitted to a hematology-oncology service where fluoroquinolone prophylaxis during neutropenia was recommended as the standard of care for many years but was then discontinued in a trial conducted in patients with acute leukemia. Fluoroquinolones had been shown to decrease the incidence of gram-negative bacteremia in cancer patients with neutropenia, yet it was thought that the emergence of resistance in Escherichia coli and other gram-negative bacteria may have caused a progressive lack of efficacy of fluoroquinolone prophylaxis. Epidemiologic surveillance of fluoroquinolone resistance of E. coli clinical isolates at our cancer center since 1992 showed a continuing influx of new clones not previously observed in the population of cancer patients, an increase in the number of cancer patients per year colonized and/or infected by fluoroquinolone-resistant E. coli (1992-1994, 10-16 patients; 1995-1997, 24-27 patients), and a resistance rate of >50% among E. coli bloodstream isolates of hematology-oncology patients. A 6-month fluoroquinolone prophylaxis discontinuation intervention trial in 1998 suggested that despite increasing resistance among E. coli isolates, fluoroquinolone prophylaxis in acute leukemia patients was still effective in the prevention of gram-negative bacteremia (incidence rates, 8% during the pre-intervention period vs. 20% after discontinuation; p<0.01). The resumption of fluoroquinolone prophylaxis in acute leukemia patients thereafter decreased the incidence of gram-negative bacteremia to the pre-intervention level (9%; p=0.03), while the proportion of in vitro fluoroquinolone resistance in E. coli bacteremia isolates again increased (from 15% during the intervention period to >50% in the post-intervention period). Relative rates of resistance thus were a poor indicator of the potential clinical benefits associated with fluoroquinolone prophylaxis in cancer patients.
Adolescent↗
High genetic variability for resistance to Bacillus thuringiensis toxins in a single population of diamondback moth.
The long-term benefit of insecticidal products based on Cry toxins, either in sprays or as transgenic crops, is threatened by the development of resistance by target pests. The models used to predict evolution of resistance to Cry toxins most often are monogenic models in which two alleles are used. Moreover, the high-dose/refuge strategy recommended for implementation with transgenic crops relies on the assumption that the resistance allele is recessive. Using selection experiments, we demonstrated the occurrence in a laboratory colony of diamondback moth of two different genes (either allelic or nonallelic) that confer resistance to Cry1Ab. At the concentration tested, resistance was dominant in one selection line and partially recessive in the other. Resistant insects from the two selection lines also differed in their cross-resistance patterns. The diamondback moth colony was derived from a field population from the Philippines, which originally showed a different resistance phenotype. This is the first time that an insect population has been directly shown to carry more than one gene conferring resistance to the same Cry toxin.
Animals↗
Evolution and mechanisms for spread of antimicrobial resistance.
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Animals↗
Chemical anatomy of antibiotic resistance: chloramphenicol acetyltransferase.
The evolution of mechanisms of resistance to natural antimicrobial substances (antibiotics) was almost certainly concurrent with the development in microorganisms of the ability to synthesise such agents. Of the several general strategies adopted by bacteria for defence against antibiotics, one of the most pervasive is that of enzymic inactivation. The vast majority of eubacteria that are resistant to chloramphenicol, an inhibitor of prokaryotic protein synthesis, owe their resistance phenotype to genes for chloramphenicol acetyltransferase (CAT), which catalyses O-acetylation of the antibiotic, using acetyl-CoA as the acyl donor. The structure of CAT is known, as are many of the properties of the enzyme which explain its remarkable specificity and catalytic efficiency. Less clear is the evolutionary pathway which has produced the different members of the CAT 'family' of enzymes. Hints come from other acetyltransferases which share structure and mechanistic features with CAT, while not being strictly 'homologous' at the level of amino acid sequence. The 'super-family' of trimeric acetyltransferases appears to have in common a chemical mechanism based on a shared architecture.
Amino Acid Sequence↗
[Evolution of Streptococcus pneumoniae antibiotic resistance in Abidjan: update on nasopharyngeal carriage, from 1997 to 2001].
UNLABELLED: The emerging antibiotic resistance and worldwide diffusion of Streptococcus pneumoniae strains is an important public health problem. OBJECTIVES: The aims of this study were to study the evolution of S. pneumoniae resistance rates to penicillin G and other antimicrobials from nasopharyngeal carriage. METHOD: Four hundred and eighty-two nasopharyngeal samples of S. pneumoniae were studied from 1997 to 2001. The Kirby-Bauer technique was used to screen the susceptibility of samples and completed with the determination of penicillin G minimal inhibitory concentration using the E-test. RESULTS: Resistance to penicillin increased from 1997 to 2001: 8.5% in 1997, 20.7% in 1998, 16% in 1999, and 23.5% in 2001. However, the resistance to other beta-lactam antibiotics was low. The rate of resistance to cotrimoxazole increased from 52.2% in 1997 to 84.3% in 2001, with a higher degree of resistance in 2001. The resistance of S. pneumoniae to tetracycline increased. In contrast, the prevalence of erythromycin-resistant pneumococcal samples decreased from 11.6% in 1997 to 8% in 2001. The resistance to three or more antibiotics (multi-drug resistant) was also increased from 9.4% in 1997 to 23.5% in 2001. CONCLUSION: This data shows that carriage of antibiotic-resistant pneumococci is increasing in Abidjan. It will be interesting to assess the current bacterial resistance patterns by a national epidemiological observatory.
Anti-Infective Agents↗
Evolution of multi-drug resistant hepatitis B virus during sequential therapy.
Multi-drug resistant hepatitis B virus (HBV) has been reported in hepatitis B patients who received sequential antiviral therapy. In vitro studies showed that HBV constructs with mutations resistant to lamivudine and adefovir have marked reduction in sensitivity to combination of lamivudine and adefovir, whereas constructs with mutations resistant to either drug remain sensitive to the other drug. We conducted this study to determine whether mutations conferring resistance to multiple antiviral agents co-locate on the same HBV genome in vivo and to describe the evolution of these mutations. Sera from six patients who had been found to have multi-drug resistant HBV mutations to lamivudine+adefovir, lamivudine+hepatitis B immunoglobulin (HBIG), or lamivudine+entecavir on direct sequencing were cloned after nested polymerase chain reaction (PCR). Analysis of 215 clones from 11 samples with multi-drug resistant mutations on direct sequencing showed that 183 (85%) clones had mutations to both therapies on the same genome; 31 clones had lamivudine-resistant mutants only. Clonal analysis of serial samples from three patients showed progressive evolution from all clones with lamivudine-resistant HBV mutations only to mixtures of clones that have multi-drug resistant mutations and clones that have lamivudine-resistant HBV mutations only, and ultimately all clones having multi-drug resistant HBV mutations. In conclusion, mutations conferring resistance to multiple antiviral agents co-locate on the same viral genome, suggesting that combination therapy directed against mutants resistant to each treatment may not be adequate in suppressing multi-drug resistant HBV. De novo combination therapy may prevent the emergence of multi-drug resistant mutants.
Adult↗
The character or the variation: the genetic analysis of the insecticide-resistance phenotype.
In this critique it is argued that the genetic basis of the evolution of resistance is dependent on how the phenotypic, and underlying genotypic, variation is channelled during a selective response. A polygenic response is preferentially favoured if selection acts within the phenotypic distribution of susceptibles; a monogenic response is predicted if selection screens rare mutations with phenotypes outside that susceptible distribution. The relevance of this model to the method of genetic analysis, the prediction of resistance mechanisms to novel insecticides, the generation of resistant beneficial insects and the development of the most effective resistance and integrated pest management programmes is discussed.
Animals↗