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23 results for “phage resistance”
Phage selection drives resistance-virulence trade-offs in Ralstonia solanacearum plant pathogenic bacterium irrespective of the growth temperature
<p><span>While temperature has been shown to affect the survival and growth of bacteria and their phage parasites, it is unclear if trade-offs between phage resistance and other bacterial traits depend on the temperature. Here, we experimentally compared the evolution of phage resistance-virulence trade-offs and underlying molecular mechanisms in phytopathogenic <em>Ralstonia</em> <em>solanacearum</em> bacterium at 25 °C and 35 °C temperature environments. We found that experimental growth conditions selected for small colony variants (SCVs) with increased growth rate and mutations in the quorum-sensing (QS) signalling receptor gene, <em>phcS</em>. Interestingly, SCVs were also phage-resistant and reached higher frequencies in the presence of phages in both temperature environments. Evolving phage resistance was costly in terms of reduced carrying capacity, biofilm formation and reduced virulence i<em>n planta</em> possibly due to loss of QS-mediated expression of key virulence genes. We also observed mucoid phage-resistant colonies that showed loss of virulence and reduced twitching motility likely due to parallel mutations in prepilin peptidase gene pilD. Moreover, phage-resistant SCVs from 35 °C-phage treatment had parallel mutations in genes encoding type II secretion system (T2SS) genes (<em>gspE</em> and <em>gspF</em>), indicating that defects in pseudopilus made bacterium resistant to the phage. Additional transcriptomic analysis revealed upregulation of CBASS and type Ⅰ restriction-modification phage defence systems in response to phage exposure, which coincided with reduced expression of motility and virulence-associated genes, including <em>pilD</em> and type II and III secretion systems. Together, these results suggest that phage resistance-virulence trade-offs are not affected by the growth temperature but can be mediated through both pre- and post-infection phage resistance mechanisms.</span></p>
Phage selection drives resistance-virulence trade-offs in Ralstonia solanacearum plant pathogenic bacterium irrespective of the growth temperature
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Higher phage virulence accelerates the evolution of host resistance
<p>Pathogens vary strikingly in their virulence and the selection they impose on their hosts. While the evolution of different virulence levels is well studied, the evolution of host resistance in response to different virulence levels is less understood and as of now mainly based on observations and theoretical predictions with few experimental tests. Increased virulence can increase selection for host resistance evolution if resistance costs are outweighed by the benefits of avoiding infection. To test this, we experimentally evolved the bacterium <em>Vibrio alginolyticus</em> in the presence of two variants of a filamentous phage that differ in their virulence. The bacterial host exhibited two alternative defence strategies: (1) super infection exclusion (SIE) whereby phage-infected cells were immune to subsequent infection at a cost of reduced growth, and (2) surface receptor mutations (SRM) providing resistance to infection by preventing phage attachment. While SIE emerged rapidly against both phages, SRM evolved faster against the high compared to the low virulence phage. Using a mathematical model of our system we show that increasing virulence strengthens selection for SRM due to the higher costs of infection suffered by SIE immune hosts. Thus, by accelerating the evolution of host resistance, more virulent phages caused shorter epidemics.</p>
Higher phage virulence accelerates the evolution of host resistance
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Data from: Phage resistance evolution in vitro is not reflective of in vivo outcome in a plant-bacteria-phage system
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Temporal shifts in antibiotic resistance elements govern phage-pathogen conflicts
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Data from: Fight evolution with evolution: plasmid-dependent phages with a wide host range prevent the spread of antibiotic resistances
The emergence of pathogenic bacteria resistant to multiple antibiotics is a serious worldwide public health concern. Whenever antibiotics are applied, the genes encoding for antibiotic resistance are selected for within bacterial populations. This has led to the prevalence of conjugative plasmids that carry resistance genes and can transfer themselves between diverse bacterial groups. In this study, we investigated whether it is feasible to attempt to prevent the spread of antibiotic resistances with a lytic bacteriophage, which can replicate in a wide range of gram-negative bacteria harboring conjugative drug-resistance conferring plasmids. The counter-selection against the plasmid was shown to be effective, reducing the frequency of multi-resistant bacteria that formed via horizontal transfer by several orders of magnitude. This was true also in the presence of an antibiotic against which the plasmid provided resistance. Majority of the multi-resistant bacteria subjected to phage selection also lost their conjugation capability. Overall this study suggests that, while we are obligated to maintain the selection for the spread of the drug resistances, the 'fight evolution with evolution' approach could help us even out the outcome to our favor.
Data from: Lytic phages obscure the cost of antibiotic resistance in Escherichia coli
The long-term persistence of antibiotic-resistant bacteria depends on their fitness relative to other genotypes in the absence of drugs. Outside the laboratory, viruses that parasitize bacteria (phages) are ubiquitous, but costs of antibiotic resistance are typically studied in phage-free experimental conditions. We used a mathematical model and experiments with Escherichia coli to show that lytic phages strongly affect the incidence of antibiotic resistance in drug-free conditions. Under phage parasitism, the likelihood that antibiotic-resistant genetic backgrounds spread depends on their initial frequency, mutation rate and intrinsic growth rate relative to drug-susceptible genotypes, because these parameters determine relative rates of phage-resistance evolution on different genetic backgrounds. Moreover, the average cost of antibiotic resistance in terms of intrinsic growth in the antibiotic-free experimental environment was small relative to the benefits of an increased mutation rate in the presence of phages. This is consistent with our theoretical work indicating that, under phage selection, typical costs of antibiotic resistance can be outweighed by realistic increases in mutability if drug resistance and hypermutability are genetically linked, as is frequently observed in clinical isolates. This suggests the long-term distribution of antibiotic resistance depends on the relative rates at which different lineages adapt to other types of selection, which in the case of phage parasitism is probably extremely common, as well as costs of resistance inferred by classical in vitro methods.
Data from: Exposure to phages has little impact on the evolution of bacterial antibiotic resistance on drug concentration gradients
The use of phages for treating bacterial pathogens has recently been advocated as an alternative to antibiotic therapy. Here we test a hypothesis that bacteria treated with phages may show more limited evolution of antibiotic resistance as the fitness costs of resistance to phages may add to those of antibiotic resistance, further reducing the growth performance of antibiotic-resistant bacteria. We did this by studying the evolution of phage-exposed and phage-free Pseudomonas fluorescens cultures on concentration gradients of single drugs, including cefotaxime, chloramphenicol, and kanamycin. During drug treatment, the level of bacterial antibiotic resistance increased through time, and was not affected by the phage treatment. Exposure to phages did not cause slower growth in antibiotic-resistant bacteria, although it did so in antibiotic-susceptible bacteria. We observed significant reversion of antibiotic resistance after drug use being terminated, and the rate of reversion was not affected by the phage treatment. The results suggest that the fitness costs caused by resistance to phages are unlikely to be an important constraint on the evolution of bacterial antibiotic resistance in heterogeneous drug environments. Further studies are needed for the interaction of fitness costs of antibiotic resistance with other factors.
Selection for phage resistance reduces virulence of Shigella flexneri
<p>There is increasing interest in phage therapy as an alternative to chemical antibiotics for treating bacterial infections, especially using phages that select for evolutionary trade-offs between increased phage resistance and decreased fitness traits such as virulence in target bacteria. A vast repertoire of virulence factors allows the opportunistic bacterial pathogen, <i>Shigella flexneri</i>, to invade human gut epithelial cells, to replicate intracellularly, and to evade host immunity through intercellular spread; the latter is an infection stage that causes tissue damage, contributing to host mortality. It is previously shown that outer membrane porin OmpA of <i>S. flexneri</i> is necessary for polar localization of virulence factor IcsA, which polymerizes host actin and results in bacterial motility within infected cells. We hypothesized that a phage which uses OmpA as a receptor to recognize, bind and infect <i>S. flexneri</i>, should select for phage-resistant mutants with attenuated intercellular spread. Here we show that a naturally-isolated <i>Myoviridae</i> virus, phage A1-1, requires OmpA as a receptor, and selects for reduced virulence in <i>S. flexneri</i>. We characterized five phage-resistant mutants by measuring their phenotypic changes relative to wildtype bacteria in various traits: cell-membrane permeability, total lipopolysaccharide (LPS), sensitivity to four antibiotics, and susceptibility to infection by phages T7 and 60B. Results separated the mutants into two groups: R1 and R2 phenotypically resembled <i>ompA</i> knockouts, whereas R3, R4 and R5 were similar to LPS-deficient strains. Whole genome sequencing confirmed that R1 and R2 had mutations in <i>ompA</i>, while R3, R4 and R5 showed mutations in LPS inner-core biosynthesis genes <i>gmhA</i> and <i>gmhC</i>. Bacterial plaque assays in Vero cells confirmed that all five phage-resistant mutants were incapable of intercellular spread. We concluded that selection for <i>S. flexneri</i> resistance to phage A1-1 generally reduced the virulence trait intercellular spread, but this trade-off could be mediated either by mutations in <i>ompA</i> or those in LPS-core genes that likely altered OmpA conformation.</p>
Data from: The cost of phage resistance in a plant pathogenic bacterium is context-dependent
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Data from: Fight evolution with evolution: plasmid-dependent phages with a wide host range prevent the spread of antibiotic resistances
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Data from: Rapid evolution of generalised resistance mechanisms can constrain the efficacy of phage-antibiotic treatments
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Data from: Exposure to phages has little impact on the evolution of bacterial antibiotic resistance on drug concentration gradients
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Evolution of bacterial cross-resistance to lytic phages and albicidin antibiotic
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Data from: Associations among antibiotic and phage resistance phenotypes in natural and clinical Escherichia coli isolates
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Selection for phage resistance reduces virulence of Shigella flexneri
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Data from: Targeting antibiotic resistant bacteria with phages reduces bacterial density in an insect host
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Data from: Pre-adapting parasitic phages to a pathogen leads to increased pathogen clearance and lowered resistance evolution with Pseudomonas aeruginosa cystic fibrosis bacterial isolates
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Data from: Lytic phages obscure the cost of antibiotic resistance in Escherichia coli
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