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At least 217 records · Page 12Linked to original sources
PubMed1988

[Evolution of bacterial resistance to five aminoglycosides. A study of 3,354 strains isolated in a hospital milieu].

The authors studied the susceptibility to 5 aminoglycosides (amikacin, dibekacin, gentamicin, netilmicin and tobramycin) of 3,354 strains isolated at the Centre Hospitalier Sud in Bordeaux during 1987. The results are compared to those obtained in 1984 on 2,818 strains. Amikacin remains the most active aminoside against the Enterobacteriaceae and Acinetobacter; against Pseudomonas, tobramycin has become the best one at that time, as well as netilmicin against Staphylococcus aureus. Evolution: no significative increase of Enterobacteriaceae resistance to aminoglycosides was observed during the last 3 years except for Providencia and Serratia. For Acinetobacter and Pseudomonas, percentage of resistant strains is respectively two-fold and three-fold higher. Although resistance increased in that species, netilmicin and amikacin showed a still good activity against Staphylococcus aureus.

Acinetobacter↗
PubMed1995

[Interaction between anti-infective agents and phagocytes].

Metchnikoff was one of the first to suggest the need for cooperation between phagocytes and therapeutic agents for the benefit of health. After the hopes raised by the discovery and the tremendous development of antimicrobials, there is now a creeping pessimism faced with the parallel evolution of resistance strategies in the microbial world. Interest has now turned to the use of immunomodulatory drugs, alone or combined with anti-infectious agents. Another tendency is based on the possibility that antimicrobials directly interfere with the host-microbe interplay. This review is aimed at summarizing our knowledge of the interactions between antimicrobial agents and the phagocyte, still a cornerstone in the natural defence system. Despite the problems inherent in the analysis and clinical relevance of effects observed in the test tube this developing area of research could provide new therapeutic solutions beyond the year 2000.

Anti-Infective Agents↗
PubMed1995

[Antibiotic resistance--an ambivalence of attitudes. As of now, the bacteria are in advantage].

The value of the precious medical asset that antibiotics constitute is contimualby being eroded by the spread of resistance. For some time that bacterial world has been adapting itself to contend with the toxic assault of man-made poisons, antibiotics, by developing resistance in a very rapid process of evolutionary changes occurring before our very eyes. This evolutionary adaptation is an example of natural genetic engineering entailing an interchange between bacteria of genes conferring antibiotic resistance. Trimethoprim resistance is an example where numerous genes of unknown origin (some closely interrelated), expressing drug-resistant dihydrofolate reductases, move among human commensals and pathogens. They have been shown to move as gene cassettes in and out of the recently characterised integron structure occurring in many pathogens. They are also carried by various transposons such as Tn7, or Tn5393 originally observed in a plant pathogen, Erwinia amylovora. Betalactam resistance is another example of natural genetic engineering, where new betalactamases are continually emerging, and individual enzyme substrate specificity is modified by point mutation. At present, betalactamase mutants resistant to all commercially available betalactams, including clavulanic acid used in combination with betalactam antibiotics, are to be found in clinical isolates. Thus, currently bacteria seem to be triumphing in the running battle between the pharmaceutical industry and the bacterial world, the former introducing one new antibiotic variant after another, to which bacteria promptly develop resistance by manipulating their own genomes.

Animals↗
PubMed1998

[Bacterial resistance to antibiotics, an exemplary model of directed molecular evolution].

The simplest conceivable event that can occur at the gene level can result in the development of efficacious resistance tot antibiotics. The bacterial world behaves as an enormous organism whose cells can exchange their genes very easily. Accordingly, opportunities for the exchange of genetic material in nature are probably unlimited. This knowledge cannot be ignored. It leads to the important conclusion that the antibiotics are societal drugs. A resistance gene which has appeared somewhere in the world can travel far and fast.

Anti-Bacterial Agents↗
PubMed1987

[Erythrocyte sedimentation rate and serum immunoglobulins in rheumatic pelvispondylitis].

Blood sedimentation rate and balanced titration of immunoglobulins were studied in 59 patients presenting a ankylosing pelvispondylitis: in 30 of them, these examinations were repeated at an interval of 3-6 months. The sedimentation rate (Sed. rate) and the level of immunoglobulins G and A increased in the course of the disease, but an elective increase of the level of immunoglobulins A was not demonstrated. Neither the Sed. rate, nor the level of IgA are correlated to evolution criteria of the disease; a positive correlation is only found with the platelets number, in a vertical study of 59 patients. Nevertheless, the variations of the immunoglobulins A is positively correlated with alterations of the clinical condition as demonstrated in the longitudinal study carried out in 30 patients. This finding supports physiopathological hypothesis which incriminates microbial intestinal infections at the origin of evolutive bouts of ankylosing pelvispondylitis.

Arthritis, Rheumatoid↗
PubMed2026

Cross-domain cooperation drives nutrient acquisition and metabolism in the bark beetle holobiont.

Microbial symbiosis underpins host adaptation, yet mechanisms of metabolic integration in holobionts remain unclear. Using metatranscriptomics, genomics, and metabolic assays, we investigated gut microbiome interactions in the European spruce bark beetle (Ips typographus). We observed metabolic complementarity among symbionts and host, forming cross-domain networks that support nutrient acquisition. Nitrogen recycling revealed strong interdependence: no single partner possessed a complete uric acid degradation pathway, but combined evidence supports a distributed pathway spanning beetle, Bacteria, and fungi. Additionally, bacterial nitrate reduction to ammonia indicates a potential nitrogen influx, making otherwise inaccessible inorganic nitrogen available to the host. Shaped by microbial interactions, symbionts also likely supply specific amino acids, while vitamin metabolism showed cross-domain co-metabolism, with Bacteria as main producers of B vitamins, while host and fungi modulated interconversion. Carbohydrate degradation was highly partitioned; bacteria target xylan and pectin, while fungi contribute to glucan breakdown. Crucially, our data provide indirect evidence that the beetle may contribute to complete cellulose degradation, highlighting an underappreciated host role in lignocellulose processing. In terms of enzymatic functional diversity, the bacteriome emerged as the most important microbiome component-an observation that contrasts with the traditional focus on fungi and underscores the need to consider bacterial contributions in insect symbioses. Despite life-stage variation, core metabolic functions remained stable. Overall, metabolic interdependence, rather than microbial composition alone, structures holobiont function. These results highlight functional redundancy and ecological resilience, emphasizing the importance of microbial cooperation and host-microbe metabolic evolution.

Bark beetle↗
PubMed1999

Antibiotic resistance and maxillofacial pathogens: emerging treatment issues.

The practice of using antibiotics to treat and control microbial infections is a little more than 50 years old. Widespread administration of multiple classes of antibiotics over the years has had the unfortunate secondary effect of inducing the emergence of an increasing array of drug-resistant microbial strains. This article will discuss the evolution of certain forms of antibiotic resistance, as well as the mechanisms by which bacteria render numerous antimicrobials ineffective. Special emphasis is placed on emerging issues relating to organisms making up portions of the normal oral microflora.

Anti-Bacterial Agents↗
PubMed1996

Metabolic efficiency and turnover of soil microbial communities in biodegradation tests.

Biodegradability screening tests of soil commonly measure 14CO2 evolution from radiolabeled test compounds, and glucose has often served as a positive control. When constant amounts of radiolabel were added to soil in combination with increasing amounts of unlabeled substrates, glucose and some related hexoses behaved in an anomalous manner. In contrast to that of formate, benzoate, n-hexadecane, or bis(2-ethylhexyl) phthalate, dilution of glucose radiocarbon with unlabeled glucose increased rather than decreased the rate and extent of 14CO2 evolution. [14C]glucose incorporation into biomass and Vmax values were consistent with the interpretation that application of relatively high concentrations of glucose to soil shifts the balance of the soil microbial community from the autochthonous (humus-degrading) to the zymogeneous (opportunistic) segment. The higher growth and turnover rates that define zymogeneous microorganisms, combined with a lower level of carbon incorporation into their biomass, result in the evolution of disproportionate percentages of 14CO2. When used as positive controls, glucose and related hexoses may raise the expectations for percent 14CO2 evolution to levels that are not realistic for other biodegradable compounds.

Biodegradation, Environmental↗
PubMed1980

Atmospheric constraints on the evolution of metabolism.

Earth's early history may have been characterized by coevolution of microbial metabolism and atmospheric composition. Metabolic developments affected the composition of the atmosphere and the resultant changes in the atmosphere stimulated the evolution of new metabolic capabilities. The first organisms were presumably fermenting heterotrophs, exploiting organic molecules abiotically synthesized. These organisms multiplied, developing new biosynthetic capabilities to overcome deficiencies in the abiotic supply of particular compounds, until their growth was limited by the energy source provided by abiotic synthesis of fermentable organic compounds. Further growth required a new energy source, which may have been the chemical energy represented by the mixture of carbon dioxide and hydrogen in the primitive atmosphere. Chemotrophic organisms resembling methane bacteria may have evolved to exploit this source. They would have flourished, along with the heterotrophs that fed on them, until they had decreased the level of atmospheric hydrogen to the point where further extractions of chemical energy from the atmosphere was not possible. Once again, the expansion of life was limited by the availability of energy. The origin of bacterial photosynthesis overcame the second energy crisis. Photosynthetic bacteria could exploit the abundant energy of sunlight while using atmospheric hydrogen and reduced compounds derived from it only as electron donors. Life flourished again, drawing atmospheric hydrogen (replenished only by volcanoes) down to levels so low as to limit even bacterial photosynthesis. Before the full potential of photosynthesis could be exploited the evolution of the metabolic apparatus to process an electron donor of unlimited abundance was necessary. This donor, of course, was water, and the new metabolic process was algal photosynthesis. The oxygen released changed the world from anaerobic to aerobic and made possible the last great advance in energy-yielding metabolism, aerobic respiration.

Aerobiosis↗
PubMed1998

Altered drug sensitivity, fitness, and evolution of human immunodeficiency virus type 1 with pol gene mutations conferring multi-dideoxynucleoside resistance.

Investigations were done to determine whether the replication kinetics of human immunodeficiency virus (HIV)-1 were altered when the virus acquired a set or subsets of five mutations (A62V, V75I, F77L, F116Y, and Q151M) in the pol gene conferring resistance to multiple dideoxynucleosides. In the absence of drugs, the replication rate of all infectious clones generated was comparable to that of wild type HIV-1. However, in the presence of zidovudine or didanosine, the comparative order for replication was HIV-1(62/75/77/116/151) > HIV-1(77/116/151) > HIV-1(75/77/116/151) approximately HIV-1(151), whereas that for drug resistance was HIV-1(75/77/116/151) > HIV-1(62/75/77/116/151) > or = HIV-1(77/116/151) > HIV-1(151). The virologic features of these infectious mutants suggest that HIV-1 develops drug resistance through one or more mutations, which, however, sacrifice replicative capability; then it finally acquires optimal replication competence by additional mutations when the multi-dideoxynucleoside-resistant mutant emerges.

Animals↗
PubMed1993

Evolutionary comparisons of three enzymes of the threonine biosynthetic pathway among several microbial species.

As an approach in the study of the evolution of threonine biosynthetic pathways throughout various organisms, the sequences of three enzymes, namely homoserine dehydrogenase, homoserine kinase and threonine synthase, originating from six organisms, namely Escherichia coli, Bacillus subtilis, Corynebacterium glutamicum, Brevibacterium lactofermentum, Pseudomonas aeruginosa and Saccharomyces cerevisiae, were compared. As a general trend all three enzymatic activities were carried out by proteins sharing sequence relatedness (except for the homoserine kinase of P aeruginosa). Unexpectedly however, for each step one or two enzymes stood out of the main stream: i) for homoserine dehydrogenase, the yeast protein is atypically similar to the E coli enzyme; ii) for homoserine kinase, the P aeruginosa protein shares no similarity with any other species; and iii) for threonine synthase, the B subtilis protein is far distant from the enzymes of other species. Hence in contrast to other biosynthetic pathways such as the tryptophan one, the threonine pathway seems not to have evolved as a whole throughout different organisms but rather each step seems to have been subjected to multiple constraints including substrate-mediated ones and host-specific ones.

Amino Acid Sequence↗
PubMed1999

How antibiotics cause antibiotic resistance.

Antimicrobial agents are approaching the end of their effectiveness. The prevailing drug development strategy is based on a presumption that results in resistance: that disease can be cured by exploitation of the vulnerabilities in microbial reproduction. Although some did predict the evolution of resistance to such drugs, the mechanisms by which genes conferring resistance have spread was not predicted. The author argues that the mechanism of spread is a consequence of the chemotherapeutics themselves acting on the evolution of pathogens, and that for future drugs to remain effective they must avoid such effects.It is thus not the individual who forms language; it is the language which forms the individual. -Alberto to Sophie in Sophie's World [Gaarder, J. (1995) Phoenix House, London]

Journal Article↗
PubMed2026

Nonantibiotic-driven evolution reveals rare but predictable routes to broad antibiotic resistance.

Many medications not prescribed to treat infectious diseases have antibacterial activity at physiologically relevant concentrations, raising the risk that chronic administration of such nonantibiotics may inadvertently select for resistance in the host microbiome. However, how frequently such exposures select for adaptations that impact broad drug resistance, including to antibiotics, remains unclear. Here, we systematically evolved Escherichia coli under exposure to 40 antibiotics and nonantibiotics and profiled the cross-resistance of the drug-adapted strains to 21 antibiotics representing all major classes. Our measurements revealed that most drug-adapted strains did not become multidrug resistant. However, five nonantibiotics and three antibiotics emerged as exceptions and were repeatedly selected for broad antibiotic resistance. Whole-genome sequencing of all 168 evolved strains revealed that changes in the regulation of efflux pumps repeatedly underlay broad drug resistance and converged into two key regulatory genes, acrR and lon. Our work suggests that although inadvertent antibiotic cross-resistance is rare, specific nonantibiotics can still potentially pose a risk for the emergence of multidrug resistance.IMPORTANCEMany medications not typically prescribed to treat infectious diseases have potent antimicrobial activity at physiological concentrations. This anti-bacterial activity raises concern that long-term administration of such nonantibiotics might unintentionally select for multidrug resistance, including resistance to antibiotics. Using Escherichia coli, we show that in most cases, these nonantibiotics do not broadly select for resistance to antibiotics in vitro. However, we identified five nonantibiotics that repeatedly selected for resistance to multiple antibiotics through a shared mechanism of action-upregulation of the multidrug efflux pump AcrAB-TolC. These findings highlight that while the overall risk is low, certain nonantibiotics may still contribute to the emergence of multidrug resistance. Identifying these high-risk drugs can help guide safer prescribing practices and inform strategies to limit the spread of antibiotic resistance.

Escherichia coli↗