[Polymicrobial infections: ecosystems with special properties]. / Polymicrobiële infecties: ecosystemen met bijzondere eigenschappen.

Bacteria often live together in complex communities. Insight into these microbial ecosystems is essential to make it possible to intervene when these ecosystems lead to disease. Bacteria do not only respond to their host, but they also affect each other, which may have far-reaching consequences for the course of the disease. In this article we describe that clinical isolates in a polymicrobial infection can be seen as ecosystems. These ecosystems often have properties that separate isolates do not have; they may, for example, be more virulent or more resistant to antibiotics. We therefore emphasise that the whole is greater than the sum of its parts, even for infections.

Nanowire sensors monitor bacterial growth kinetics and response to antibiotics.

Miniaturized and cost-efficient methods aiming at high throughput analysis of microbes are of great importance for the surveillance and control of infectious diseases and the related issue of antimicrobial resistance. Here we demonstrate a miniature nanosensor based on a honeycomb-patterned silicon nanowire field effect transistor (FET) capable of detection of bacterial growth and antibiotic response in microbiologically relevant nutrient media. We determine the growth kinetics and metabolic state of Escherichia coli cells in undiluted media via the quantification of changes in the source-drain current caused by varying pH values. Furthermore, by measuring the time dependent profile of pH change for bacterial cultures treated with antibiotics, we demonstrate for the first time the possibility of electrically distinguishing between bacteriostatic and bactericidal drug effects. We believe that the use of such nanoscopic FET devices enables addressing parameters that are not easily accessible by conventional optical methods in a label-free format, i.e. monitoring of microbial metabolic activity or stress response.

Experimental tests of host-virus coevolution in natural killer yeast strains.

Fungi may carry cytoplasmic viruses that encode anticompetitor toxins. These so-called killer viruses may provide competitive benefits to their host, but also incur metabolic costs associated with viral replication, toxin production and immunity. Mechanisms responsible for the stable maintenance of these endosymbionts are insufficiently understood. Here, we test whether co-adaptation of host and killer virus underlies their stable maintenance in seven natural and one laboratory strain of the genus Saccharomyces. We employ cross-transfection of killer viruses, all encoding the K1-type toxin, to test predictions from host-virus co-adaptation. These tests support local adaptation of hosts and/or their killer viruses. First, new host-virus combinations have strongly reduced killing ability against a standard sensitive strain when compared with re-constructed native combinations. Second, viruses are more likely to be lost from new than from original hosts upon repeated bottlenecking or the application of stressful conditions. Third, host fitness is increased after the re-introduction of native viruses, but decreased after the introduction of new viruses. Finally, rather than a trade-off, original combinations show a positive correlation between killing ability and fitness. Together, these results suggest that natural yeast killer strains and their viruses have co-adapted, allowing the transition from a parasitic to a mutualistic symbiosis.

Limits to adaptation in asexual populations.

In asexual populations, the rate of adaptation is basically limited by the frequency and properties of spontaneous beneficial mutations. Hence, knowledge of these mutational properties and how they are affected by particular evolutionary conditions is a precondition for understanding the process of adaptation. Here, we address how the rate of adaptation of asexual populations is limited by its population size and mutation rate, as well as by two factors affecting the fraction of mutations that confer a benefit, i.e. the initial adaptedness of the population and the variability of the environment. These factors both influence which mutations are likely to occur, as well as the probability that they will ultimately contribute to adaptation. We attempt to separate the consequences of these basic population features in terms of their effect on the rate of adaptation by using results from evolution experiments with microorganisms.

TEST OF INTERACTION BETWEEN GENETIC MARKERS THAT AFFECT FITNESS IN ASPERGILLUS NIGER.

In this paper we study whether and how a number of arbitrarily chosen marker mutations interact in their effect on fitness, which is relevant for our understanding of the evolution of sex. If epistasis is synergistic, the main function of sex may be to facilitate selection against deleterious mutations. We use strains of the filamentous fungus Aspergillus niger with variable combinations of marker mutations that have been obtained by isolating segregants from a diploid between a wild-type strain and a related strain carrying a marker mutation on each of its eight chromosomes. The marker mutations include five auxotrophic and two resistance mutations. As a measure of fitness the mycelium growth rate on supplemented medium has been used. The results suggest that the marker mutations have independent effects on fitness, and hence they do not support the deterministic mutation hypothesis of the evolution of sex. The apparent linear relationship between mutation number and log fitness is the result of interactions of opposite type (i.e., synergistic and antagonistic) that cancel each other's effect. However, due to an isolation bias caused by the fact that not all possible strains with many mutations could be isolated, the results may be relatively biased towards an antagonistic relationship between mutation number and log fitness.