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PubMed2004

Molecular basis of the evolution of drug resistance: potential role of the transient state during infection/drug treatment.

Transient period represents the time window between the exposure and response to the given stimuli inflicting the stress on the host. However, this time window is unlikely to engage in variety of signaling to culminate drastic impact on the host cell rather it is evolutionary in its sense implying a slow process. But it is reasonable to speculate that most significant signals are initiated at this time, and first responder will confer required adaptive features on the host cells. This alteration would be followed by amplification of appropriate adaptative signals in the successive generation(s), thus conferring the increased adaptability to given stress.

Adaptation, Physiological↗
PubMed2004

Somatic mutation-mediated evolution of herbicide resistance in the nonindigenous invasive plant hydrilla (Hydrilla verticillata).

Hydrilla (Hydrilla verticillata L.f. Royle) was introduced to the surface water of Florida in the 1950s and is today one of the most serious aquatic weed problems in the USA. As a result of concerns associated with the applications of pesticides to aquatic systems, fluridone is the only USEPA-approved chemical that provides systemic control of hydrilla. After a decrease in fluridone's efficacy at controlling hydrilla, 200 Florida water bodies were sampled to determine the extent of the problem and the biological basis for the reduced efficacy. Our studies revealed that hydrilla phenotypes with two- to six-fold higher fluridone resistance were present in 20 water bodies. Since fluridone is an inhibitor of the enzyme phytoene desaturase (PDS), the gene for PDS (pds) was cloned from herbicide-susceptible and -resistant hydrilla plants. We report for the first time in higher plants three independent herbicide-resistant hydrilla biotypes arising from the selection of somatic mutations at the arginine 304 codon of pds. The three PDS variants had specific activities similar to the wild-type enzyme but were two to five times less sensitive to fluridone. In vitro activity levels of the enzymes correlated with in vivo resistance of the corresponding biotypes. As hydrilla spread rapidly to lakes across the southern United States in the past, the expansion of resistant biotypes is likely to pose significant environmental challenges in the future.

Base Sequence↗
PubMed2002

Mutation and evolution of antibiotic resistance: antibiotics as promoters of antibiotic resistance?

Antibiotic resistance appearance and spread have been classically considered the result of a process of natural selection, directed by the use of antibiotics. Bacteria, that have to face the antibiotic challenge, evolve to acquire resistance and, under this strong selective pressure, only the fittest survive, leading to the spread of resistance mechanisms and resistant clones. Horizontal transference of resistance mechanisms seems to be the main way of antibiotic resistance acquisition. Nevertheless, recent findings on hypermutability and antibiotic-induced hypermutation in bacteria have modified the landscape. Here, we present a review of the last data on molecular mechanisms of hypermutability in bacteria and their relationship with the acquisition of antibiotic resistance. Finally, we discuss the possibility that antibiotics may act not only as selectors for antibiotic resistant bacteria but also as resistance promoters.

Adaptation, Physiological↗
PubMed1999

Evolution of resistance among clinical isolates of Acinetobacter over a 6-year period.

The aim of this report was to study the evolution of susceptibilities of 1532 clinical isolates of Acinetobacter recovered over a period of 6 years. The minimal inhibitory concentrations (MICs) of 15 antimicrobial agents were determined for all the isolates. The respective percentages of resistant strains in the years 1991 and 1996 were as follows: ciprofloxacin, 54.4% and 90.4%; tobramycin, 33% and 71.8%; amikacin, 21% and 83.7%; ampicillin plus sulbactam, 65.7% and 84.1%; ceftazidime, 57.4% and 86.8%; ticarcillin, 70% and 89.4%; trimethoprim plus sulfamethoxazole, 41.1% and 88.9%; and imipenem, 1.3% and 80%. The MIC90s of ciprofloxacin, sparfloxacin, biapenem, meropenem, imipenem, cefepime, cefpirome, and rifampicin against 250 imipenem-resistant Acinetobacter strains were >32, >32, 128, >256, 256, >256, 256, and 16 mg/l, respectively. With serious infections, it was necessary to resort to the use of colistin, the only antibiotic active in vitro.

Acinetobacter↗
PubMed1997

The within-host population dynamics of antibacterial chemotherapy: conditions for the evolution of resistance.

For tuberculosis and number of other bacterial infections, treatment with a single antimicrobial drug frequently fails due to the ascent of mutants resistant to that drug. To minimize the likelihood of this occurrence, multiple drugs with independent resistance mechanisms are used simultaneously. None the less, multiply resistant bacteria sometimes emerge even when patients are simultaneously treated with two or more drugs, and the ascent of these multiply-resistant mutants may result in treatment failure in the patient and spread of these resistant bacteria to other hosts. We consider two mathematical models of antibacterial chemotherapy which can account for the ascent of multiple antibiotic resistance within hosts treated with multiple antibiotics. In both, multiple resistance evolves because of selection favouring mutants resistant to fewer than all of the chemotherapeutic agents employed, intermediates. In one model, this occurs because of temporal fluctuations in the concentrations of the antibiotics in the course of normal treatment and/or because of non-adherence to the treatment regime. In the other, intermediates are favoured and multiple resistance evolves because of tissue and somatic cell heterogeneity. In the effective concentrations of the antibiotics and physiological variation in the sensitivity of subpopulations of bacteria to different antibiotics. We discuss the limitations (and assets) of this model and approach and the implications for the design of antibiotic treatment regimes. Finally, we consider how the assumptions behind this model and the predictions made from its analysis could be tested experimentally.

Animals↗
PubMed2002

Heritable variation of sex pheromone composition and the potential for evolution of resistance to pheromone-based control of the Indian meal moth, Plodia interpunctella.

The short-term evolutionary effect of pheromone-based mating disruption on the mating ability of the Indian meal moth, Plodia interpunctella, was investigated. Three independent selection lines were established, and the mating ability of moths in plastic tents treated with high doses of pheromone and in control tents was compared for two consecutive generations. In addition, the heritability of the sex pheromone blend, measured as the ratio of two major pheromone components (Z,E)-9,12-tetradecadienyl acetate and (Z,E)-9,12-tetradecadienol, was estimated. Based on a mother-daughter regression analysis including 21 families, the heritability of the pheromone blend was 0.65 +/- 0.14, indicating a potential for evolutionary change of the character. However, no increase in mating ability of females in pheromone-treated tents or alteration of the pheromone blend was observed in any selection line when compared with control lines, indicating no or weak selection on the pheromone blend as well as other traits influencing mating ability of this species under the created mating disruption conditions. Factors contributing to the lack of selection effects are discussed.

Animals↗
PubMed1998

The evolution of treatment resistance: biologic implications.

The evolution of resistance of positive symptoms to antipsychotic therapy may represent a valuable means of subtyping schizophrenia. In contrast, resistance of negative symptoms and cognitive function to antipsychotic agents seems to be present from the first episode of psychotic symptoms and does not evolve over time to the same extent. If these findings are validated, this clearly points toward differences in the etiology of these components of schizophrenia. Data from a cohort of 223 patients with unsatisfactory responses to classical antipsychotic therapy are evaluated, at least 60% of whom responded to subsequent treatment with clozapine. Comparisons were made between the subgroups of patients with primary and delayed onset treatment resistance. Both subgroups responded to clozapine therapy, although better response was evident for patients with delayed resistance. The withdrawal of clozapine from patients who had previously been responsive to classical antipsychotic therapy was capable of inducing treatment resistance.

Antipsychotic Agents↗
PubMed2026

Single unscreened carrier triggered ICU outbreak of a KPC-producing Klebsiella pneumoniae which acquired in vivo resistance to ceftazidime-avibactam, and cefiderocol.

BACKGROUND: Carbapenemase-producing Enterobacterales are a major cause of healthcare-associated outbreaks in intensive care units (ICUs), where unrecognized carriers can drive silent transmission. We report an ICU outbreak caused by KPC-producing Klebsiella pneumoniae and the within-host emergence of resistance to ceftazidime-avibactam and cefiderocol in the index case. METHODS: Four ICU patients with five K. pneumoniae isolates identified between July and August 2023 were investigated. Phenotypic, genomic and functional analyses were performed to determine the clonal relatedness of the isolates and elucidate the mechanisms underlying resistance evolution. RESULTS: All isolates belonged to ST512, confirming dissemination of a single high-risk clone. The first isolate recovered from the index patient was susceptible to ceftazidime-avibactam and cefiderocol, but a later isolate obtained during ceftazidime-avibactam therapy acquired resistance to both agents. Genomic analysis revealed a novel KPC variant (KPC-270) carrying a 19-amino-acid duplication. When expressed in Escherichia coli, KPC-270 conferred ceftazidime-avibactam resistance, but it did not fully reproduce the meropenem or cefiderocol phenotype. Efflux inhibition substantially reduced meropenem and cefiderocol MICs in the resistant isolate, and avibactam partially restored cefiderocol activity, supporting multifactorial mechanism. CONCLUSION: This outbreak illustrates how unrecognized multidrug-resistant carriage in the index patient facilitated the nosocomial dissemination of a high-risk ST512 K. pneumoniae clone, followed by rapid resistance evolution during ceftazidime-avibactam therapy. Resistance was multifactorial, involving the novel KPC-270 variant and efflux activity contributing to ceftazidime-avibactam, meropenem and cefiderocol resistance.

Cefiderocol↗
PubMed2004

[The evolution of plant disease resistance gene].

The evolution of plant disease resistance genes has shaped in some kinds of common forms. The duplication of plant progenitor disease resistance gene creates disease resistance gene loci. The intragenic and extragenic recombination results in variation. Recombination also is involved in generation novel resistance specificities. In addition, the leucine-rich repeats (LRRs) involved in recognitional specificity are subject to adaptive selection. Insertion of transposable elements into several resistance gene loci result in further evolution of resistance genes. With the evolution of plant disease resistance genes, the R genes (resistance genes)-mediated response shows diversification which represents different stages in the oscillating evolution between plants and their pathogens.

Adaptation, Physiological↗
PubMed2024

Decoding the trajectory of antibiotic resistance genes in saline and alkaline soils: Insights from different fertilization regimes.

The soil salinity and alkalinity play an important role in the occurrence and proliferation of antibiotic resistance genes (ARGs). Yet, little is known the underlying mechanism by which soil salinity and alkalinity affect antibiotic resistance evolution. Here we investigated the ARGs variation in soil salinity and alkalinity environments created by different fertilization, and explored the biological mechanisms that salinity and alkalinity alter the evolutionary paradigm of antibiotic resistance. The results showed the soil treated by organic fertilizer exhibited a low salinity, neutral level (TSD 239.20 μS/cm, pH 7.17). The ARG abundance in the OF treatment was the highest, keeping an average of 67.83 TPM. Beside the effect of direct input of organic fertilizer at the beginning, it was important to note that, ARGs abundance during planting showed significant correlations with pH and electric conductivity. We observed that changes in microbial survival strategies under different salinity and alkalinity conditions further affected ARG hosts abundance. Indoor experiments demonstrated that there was a survival trade-off between the growth of resistant bacteria and the evolution of antibiotic resistance in salinity and alkalinity environments. Meta-genomic and Meta-transcriptomic analysis consistently demonstrated bacterial antibiotic resistance was primarily associated with pyruvate, energy and lipid metabolic pathways. The functional gene related to salinity and alkalinity, like cysH, cysK, plsB and plsC showed negative correlations with MDR. Prokaryotic transcription assays validated these relations. This study well explains the prevalence of soil ARGs after different fertilization regimes and will give a deeper understanding for the effect of soil salinity and alkalinity on antibiotic resistance evolution.

Soil↗
PubMed2002

[Insulin resistance and evolution].

Both infections and injuries activate the immunity system, leading to a series of metabolic changes which place the organism at a disadvantage and contribute to its elimination, thus facilitating the repair of the injured tissue. The study of the actions of tumour necrosing factor alpha (TNF-alpha) and interleukin-6 (IL-6), classically implicated in inflammatory processes and in fighting infection, has revealed numerous metabolic effects. Some gene polymorphisms of TNF-alpha and IL-6 (associated with a different TNF-alpha or IL-6 transcription rate) and the plasma concentrations of the soluble TNF-alpha receptor are found to be simultaneously associated with resistance to insulin, the proportion of body fat and with the mortality linked with different chronic infections. Therefore, it seems that the immune system is designed to fight infections effectively and to provide certain survival advantages during periods of intermittent fasting so frequent in the past. By inducing a resistance to insulin in the muscles, the energy substrates would thus be reserved for neuronal metabolism. In the presence of an insulin-resistance genotype and a westernization of the environment (carbohydrate-rich diet, an increase in saturated fat, low fibre and sedentary lifestyle), a genotype with a high cytokine response will contribute to a worsening of the resistance to insulin and, finally, to type 2 diabetes mellitus and atherosclerosis. The advantages for our ancestors of a large cytokine response (eradication of the lesion) or moderate resistance to insulin (protection against food shortage) have led in the present day to the development of atherosclerosis now that the characteristics of the environment have changed. It is contended that these changes constitute examples of good adaptation to the environment or poor concordance between our current lifestyle and our genome.

Biological Evolution↗
PubMed1985

R1767, an example of the evolution of resistance plasmids.

The Salmonella R-factor system R1767 undergoes frequent rearrangement of its plasmid components. The flux of genetic material within this plasmid system depends on a combination of illegitimate and homologous recombination. The presence of several copies of IS160 and two multiresistance transposons, Tn2410 and Tn2411, are substantial reasons for the observed variations.

Biological Evolution↗
PubMed2005

CML clonal evolution with resistance to single agent imatinib therapy.

We describe a 58-year-old male diagnosed with chronic myeloid leukaemia (CML) who failed to have a cytogenetic response to interferon-alpha and hydroxyurea. On subsequent therapy with imatinib mesylate he failed to have any cytogenetic response but also developed a complex clonal evolution with an additional Philadelphia (Ph) chromosome and trisomy 8 respectively in two Ph-positive subclones. The addition of cytosine arabinoside to imatinib resulted in reversion to single Ph-chromosome positivity with the disappearance of the previous additional clonal abnormalities. The case demonstrates the efficacy of combined treatment with imatinib and cytarabine in the management of CML resistant to single agent imatinib.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

High-temperature stress and the evolution of thermal resistance in Drosophila.

The evolution of thermal resistance and acclimation is reviewed at the population level using populations and isofemale lines of Drosophila buzzatii and D. melanogaster originating from different climatic regions. In general, ample genetic variation for thermal resistance was found within and among populations. A rough correlation between the climate of origin and thermal resistance was apparent. Acclimation at a non-lethal temperature led to a significant increase in survival after heat shock, and recurrent acclimation events generally increased survival even further. Acclimation effects lasted over several days, but this effect decreased gradually with time since acclimation. Protein studies showed that the concentration of Hsp70 in adult flies is greatly increased by acclimation and thereafter gradually decreases with time. For populations with relatively high survival at one life stage, survival often was low at other life stages. Furthermore, selection on different life stages showed that a selection response in one life stage did not necessarily result in a correlated response in another. These observations indicate that different mechanisms or genes at least in part are responsible for or are expressed at different developmental stages. Selection for increased resistance was successful despite low heritabilities for the trait. Survival and fertility were compared between acclimated and non-acclimated flies, and a cost of expressing the "heat shock response" was identified in that increased survival after acclimation was accompanied by reduced fertility. The relative costs increased under nutritional stress. Metabolic rate was genetically variable but did not correlate with temperature resistance. The more resistant lines, however, often had shorter developmental time. Inbreeding reduced thermal stress tolerance of adult flies, but it did not reduce tolerance of embryos that possibly are exposed to strong natural selection for thermal stress resistance. In general, inbreeding may reduce stress resistance, and thus multiple stressful events may account for increased inbreeding depression in harsh environments.

Acclimatization↗