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Dietary restriction (DR), limiting calories or specific nutrients without malnutrition, extends lifespan across diverse taxa. Traditionally, this lifespan extension has been explained as a result of diet-mediated changes in the trade-off between lifespan and reproduction, with survival favoured when resources are scarce. However, a recently proposed alternative suggests that the selective benefit of the response to DR is the maintenance of reproduction. This hypothesis predicts that lifespan extension is a side effect of benign laboratory conditions, and DR individuals would be frailer and unable to deal with additional stressors, and thus lifespan extension should disappear under more stressful conditions. We tested this by rearing outbred female fruit flies (Drosophila melanogaster) on 10 different protein:carbohydrate diets. Flies were either infected with a bacterial pathogen (Pseudomonas entomophila), injured with a sterile pinprick or unstressed. We monitored lifespan, fecundity and measures of ageing. DR extended lifespan and reduced reproduction irrespective of injury and infection. Infected flies on lower protein diets had particularly poor survival. Exposure to infection and injury did not substantially alter the relationship between diet and ageing patterns. These results do not provide support for lifespan extension under DR being a side effect of benign laboratory conditions. This article is protected by copyright. All rights reserved.

Background Helicobacter pylori is a human gastric carcinogen that is highly prevalent in Latin American. The prophages of H. pylori show a structured population and contribute to the diversity of this bacterium. However, H. pylori prophages present in American strains have not been described to date. In this study, we identified, characterized, and present the phylogenetic analysis of the prophages present in Colombian H. pylori strains. Methods To characterize Colombian H. pylori strains and their prophages, a Multilocus Sequences Typing (MLST) and a Prophage Sequences Typing (PST), using the integrase and holin genes, were performed. Furthermore, five Colombian H. pylori had their full genome sequenced, and six Colombian H.pylori retrieved from databases, allowing to determine the prophage complete genome and insertion site. Results The integrase gene frequency was 12.6% (27/213), while both integrase and holin genes were present in 4.2% (9/213) of the samples analyzed. The PST analysis showed that Colombian prophages belong to different populations, including hpSWEurope, hpNEurope, hpAfrica1, and a new population, named hpColombia. The MLST analysis classified most of the Colombia strains in the hpEurope population. Conclusions The new H. pylori prophage population revealed that Colombian prophages follow a unique evolutionary trajectory, contributing to bacterial diversity. The global H. pylori prophage phylogeny highlighted five phylogenetic groups, one more than previously reported. After the arrival of Europeans, the Colombian H. pylori bacteria and their prophages formed an independent evolutionary line to adapt to the new environment and new human hosts.

Summary Maternal effects are increasingly recognized to impact upon infectious diseases. Stressful environmental conditions that coincide with high infection prevalence are potential cues for adaptive maternal effects on offspring resistance to infection. We studied how maternal temperature (15 °C, 20 °C and 25 °C), as well as maternal food availability (high and low food) influenced the ability of the crustacean, Daphnia magna, to resist its bacterial parasite, Pasteuria ramosa. Mothers held at a higher temperature and mothers fed a restricted diet produced offspring that were more resistant to P. ramosa infection. Maternal temperature also influenced the progression of disease in infected offspring. Parasite spore production and host reproduction were affected by maternal temperature, but these effects differed in the two genotypes used. As Daphnia populations experience regular summer epidemics of P. ramosa, temperature may be an environmental signal of infection risk. Thus, the enhanced resistance we observed under stressful food and temperature is conceivably an adaptation to looming epidemics. Thus, this study identifies novel ways in which the maternal environment impacts upon disease resistance and indicates how phenotypic plasticity might both alter co-evolution and mitigate epidemics driven by environmental change in a wide range of taxa.

Adaptation depends greatly on the distribution of mutation fitness effects (DMFE), but the phenotypic expression of mutations is often environment dependent. The environments faced by multihost pathogens are mostly governed by their hosts and therefore measuring the DMFE on multiple hosts can inform on the likelihood of short-term establishment and longer term adaptation of emerging pathogens. We explored this by measuring the growth rate of 36 mutants of the lytic bacteriophage φX174 on two host backgrounds, Escherichia coli (EcC) and Salmonella typhimurium (StGal). The DMFE showed higher mean and variance on EcC than on StGal. Most mutations were either deleterious or neutral on both hosts, but a greater proportion of mutations were deleterious on StGal. We identified two mutations with beneficial fitness effects on EcC that were neutral on StGal. Host-specific differences in fitness were associated with particular functional classes of genes involved in the initial stages of infection in accordance with previous studies of host specificity. Overall, there was a positive correlation between the effects of mutations on each host, suggesting that most new mutations will have general, rather than host-specific fitness effects. We consider these results in light of simple fitness landscape models of adaptation and discuss the relevance of context-dependent DMFE for multihost pathogens.

Epidemiology in host meta-populations depends on parasite ability to disperse between, establish and persist in distinct sub-populations of hosts. We studied the genetic factors determining the short-term establishment, and long-term maintenance, of pathogens introduced by infected hosts (i.e. carriers) into recipient populations. We used experimental populations of the freshwater ciliate Paramecium caudatum and its bacterial parasite Holospora undulata. Parasite short-term spread (approximately one horizontal transmission cycle) was affected mainly by carrier genotype, and its interactions with parasite and recipient genotypes. By contrast, parasite longer term spread (2-3 horizontal transmission cycles) was mostly determined by parasite isolate. Importantly, measures of parasite short-term success (reproductive number, R) were not good predictors for longer term prevalence, probably because of the specific interactions between host and parasite genotypes. Analogous to variation in vectorial capacity and super-spreader occurrence, two crucial components of epidemiology, we show that carrier genotype can also affect disease spread within meta-populations.

Waterborne pathogens are responsible for several diseases, either due to the consumption of contaminated drinking water or due to the contact with polluted recreational waters. There is an increasing awareness that emergent and viral pathogens should also be monitored for determining water quality. Conventional detection methodologies present several shortcomings, such as reliance in indicator species, low throughput and increasing resources as more species are to be detected. DNA chips have the potential to serve as surveillance systems for the simultaneous detection of pathogens, overcoming these limitations. In the present study, a rapid method for the detection of multiple waterborne pathogens (bacteria and viruses) was developed, using a DNA chip (AQUACHIP®). Species and group specific probes were implemented on a DNA chip, both for mandatory and non-mandatory microorganisms. Considerations regarding the AQUACHIP® design (probe layout, replicates and dilutions), DNA labelling and amplification, and preliminary results of the application of the chip for the detection of E. coli DNA are presented (© 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

The use of surveillance systems demonstrates that waterborne pathogens are responsible for several diseases associated either with consuming of contaminated drinking water or contacting polluted recreational waters. To assure water quality not only mandatory microorganisms should be screened for. Emergent pathogens that represent danger to public health should also be analysed. Culture methods used routinely in water microbiology (bacteriology) laboratories are long time consumable. Moreover some of the emergent pathogens are not represented by conventional indicator bacteria, which limit the screening power of the current methodology. The present study aims at developing a rapid method to simultaneously detect several microorganisms (bacteria, protozoa, and virus) in water samples by the use of a DNA chip (AQUACHIP). Species specific DNA probes were developed based on the data available at public genomes databases. The probes were validated against the tested microorganism and artificial contaminated waters. Validation data shows that the probes may be useful to quickly evaluate water quality. (© 2009 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)

© 2017 John Wiley & Sons Ltd., Background: Helicobacter pylori virulence is associated with different clinical outcomes. The existence of an intact dupA gene from tfs4b cluster has been suggested as a predictor for duodenal ulcer development. However, the role of tfs plasticity zone clusters in the development of ulcers remains unclear. We studied several H. pylori strains to characterize the gene arrangement of tfs3 and tfs4 clusters and their impact in the inflammatory response by infected gastric cells. Methods: The genome of 14 H. pylori strains isolated from Western patients, pediatric (n=10) and adult (n=4), was fully sequenced using the Illumina platform MiSeq, in addition to eight pediatric strains previously sequenced. These strains were used to infect human gastric cells, and the secreted interleukin-8 (IL-8) was quantified by ELISA. The expression of virB2, dupA, virB8, virB10, and virB6 was assessed by quantitative PCR in adherent and nonadherent fractions of H. pylori during in vitro co-infection, at different pH values. Results: We have found that cagA-positive H. pylori strains harboring a complete tfs plasticity zone cluster significantly induce increased production of IL-8 from gastric cells. We have also found that the region spanning from virB2 to virB10 genes constitutes an operon, whose expression is increased in the adherent fraction of bacteria during infection, as well as in both adherent and nonadherent fractions at acidic conditions. Conclusions: A complete tfs plasticity zone cluster is a virulence factor that may be important for the colonization of H. pylori and to the development of severe outcomes of the infection with cagA-positive strains., This work was supported by the FCT-PTDC/BIM-MEC/1051/2012 grant from the Fundação para a Ciência e a Tecnologia (FCT) (to M.O.). B.S. and F.F.V. are recipients of postdoctoral fellowships (PTDC/BIM- MEC/1051/2012 and SFRH/BPD/95125/2013, respectively) from FCT, and R.R is recipient of a fellowship (BRJ-DDI/2012) from the National Institute of Health. WGS and capillary sequencing were performed at Unidade de Tecnologia e Inovação (Departamento de Genética Humana, Instituto Nacional de Saúde Dr Ricardo Jorge, Lisbon, Portugal).