Superorganism resilience: eusociality and susceptibility of ecosystem service providing insects to stressors

Insects provide crucial ecosystem services for human food security and maintenance of biodiversity. Therefore, major declines in wild insects combined with losses of managed bees have raised great concern. Recent data suggest that honey bees appear to be less susceptible to stressors compared to other species. Here, we argue that eusociality plays a key role for the susceptibility of insects to environmental stressors due to superorganism resilience, which can be defined as the ability to tolerate the loss of somatic cells (= workers) as long as the germ line (= reproduction) is maintained. Life history and colony size appear critical for such resilience. Future conservation efforts should take superorganism resilience into account to safeguard ecosystem services by insects.

Communication in troubled waters: responses of fish communication systems to changing environments

Fish populations are increasingly being subjected to anthropogenic changes to their sensory environments. The impact of these changes on inter- and intra-specific communication, and its evolutionary consequences, has only recently started to receive research attention. A disruption of the sensory environment is likely to impact communication, especially with respect to reproductive interactions that help to maintain species boundaries. Aquatic ecosystems around the world are being threatened by a variety of environmental stressors, causing dramatic losses of biodiversity and bringing urgency to the need to understand how fish respond to rapid environmental changes. Here, we discuss current research on different communication systems (visual, chemical, acoustic, electric) and explore the state of our knowledge of how complex systems respond to environmental stressors using fish as a model. By far the bulk of our understanding comes from research on visual communication in the context of mate selection and competition for mates, while work on other communication systems is accumulating. In particular, it is increasingly acknowledged that environmental effects on one mode of communication may trigger compensation through other modalities. The strength and direction of selection on communication traits may vary if such compensation occurs. However, we find a dearth of studies that have taken a multimodal approach to investigating the evolutionary impact of environmental change on communication in fish. Future research should focus on the interaction between different modes of communication, especially under changing environmental conditions. Further, we see an urgent need for a better understanding of the evolutionary consequences of changes in communication systems on fish diversity.

Moving beyond a descriptive aquatic toxicology: the value of biological process and trait information

In order to improve the ability to link chemical exposure to toxicological and ecological effects, aquatic toxicology will have to move from observing what chemical concentrations induce adverse effects to more explanatory approaches, that are concepts which build on knowledge of biological processes and pathways leading from exposure to adverse effects, as well as on knowledge on stressor vulnerability as given by the genetic, physiological and ecological (e.g., life history) traits of biota. Developing aquatic toxicology in this direction faces a number of challenges, including (i) taking into account species differences in toxicant responses on the basis of the evolutionarily developed diversity of phenotypic vulnerability to environmental stressors, (ii) utilizing diversified biological response profiles to serve as biological read across for prioritizing chemicals, categorizing them according to modes of action, and for guiding targeted toxicity evaluation; (iii) prediction of ecological consequences of toxic exposure from knowledge of how biological processes and phenotypic traits lead to effect propagation across the levels of biological hierarchy; and (iv) the search for concepts to assess the cumulative impact of multiple stressors. An underlying theme in these challenges is that, in addition to the question of what the chemical does to the biological receptor, we should give increasing emphasis to the question how the biological receptor handles the chemicals, i.e., through which pathways the initial chemical-biological interaction extends to the adverse effects, how this extension is modulated by adaptive or compensatory processes as well as by phenotypic traits of the biological receptor.

Molecular crosstalk between a chemical and a biological stressor and consequences on disease manifestation in rainbow trout.

The aim of the present study was to examine the molecular and organism reaction of rainbow trout, Oncorhynchus mykiss, to the combined impact of two environmental stressors. The two stressors were the myxozoan parasite, Tetracapsuloides bryosalmonae, which is the etiological agent of proliferative kidney disease (PKD) and a natural stressor to salmonid populations, and 17β-estradiol (E2) as prototype of estrogen-active chemical stressors in the aquatic environment. Both stressors, the parasite and estrogenic contaminants, co-exist in Swiss rivers and are discussed as factors contributing to the decline of Swiss brown trout populations over the last decades. Using a microarray approach contrasting parasite-infected and non-infected rainbow trout at low or high estrogen levels, it was observed that molecular response patterns under joint exposure differed from those to the single stressors. More specifically, three major response patterns were present: (i) expression responses of gene transcripts to one stressor are weakened by the presence of the second stressor; (ii) expression responses of gene transcripts to one stressor are enhanced by the presence of the second stressor; (iii) expression responses of gene transcripts at joint treatment are dominated by one of the two stressors. Organism-level responses to concurrent E2 and parasite treatment - assessed through measuring parasite loads in the fish host and cumulative mortalities of trout - were dominated by the pathogen, with no modulating influence of E2. The findings reveal function- and level-specific responses of rainbow trout to stressor combinations, which are only partly predictable from the response to the single stressors.

Climate change and infectious diseases of wildlife: Altered interactions between pathogens, vectors and hosts

Infectious diseases result from the interactions of host, pathogens, and, in the case of vector-borne diseases, also vectors. The interactions involve physiological and ecological mechanisms and they have evolved under a given set of environmental conditions. Environmental change, therefore, will alter host-pathogen-vector interactions and, consequently, the distribution, intensity, and dynamics of infectious diseases. Here, we review how climate change may impact infectious diseases of aquatic and terrestrial wildlife. Climate change can have direct impacts on distribution, life cycle, and physiological status of hosts, pathogens and vectors. While a change in either host, pathogen or vector does not necessarily translate into an alteration of the disease, it is the impact of climate change on the interactions between the disease components which is particularly critical for altered disease risks. Finally, climate factors can modulate disease through modifying the ecological networks host-pathogen-vector systems are belonging to, and climate change can combine with other environmental stressors to induce cumulative effects on infectious diseases. Overall, the influence of climate change on infectious diseases involves different mechanisms, it can be modulated by phenotypic acclimation and/or genotypic adaptation, it depends on the ecological context of the host-pathogen-vector interactions, and it can be modulated by impacts of other stressors. As a consequence of this complexity, non-linear responses of disease systems under climate change are to be expected. To improve predictions on climate change impacts on infectious disease, we suggest that more emphasis should be given to the integration of biomedical and ecological research for studying both the physiological and ecological mechanisms which mediate climate change impacts on disease, and to the development of harmonized methods and approaches to obtain more comparable results, as this would support the discrimination of case-specific versus general mechanisms

Biochanin A and prunetin improve epithelial barrier function in intestinal CaCo-2 cells via downregulation of ERK, NF-κB, and tyrosine phosphorylation

The single-layered gut epithelium represents the primary line of defense against environmental stressors; thereby monolayer integrity and tightness are essentially required to maintain gut health and function. To date only a few plant-derived phytochemicals have been described as affecting intestinal barrier function. We investigated the impact of 28 secondary plant compounds on the barrier function of intestinal epithelial CaCo-2/TC-7 cells via transepithelial electrical resistance (TEER) measurements. Apart from genistein, the compounds that had the biggest effect in the TEER measurements were biochanin A and prunetin. These isoflavones improved barrier tightness by 36 and 60%, respectively, compared to the untreated control. Furthermore, both isoflavones significantly attenuated TNFα-dependent barrier disruption, thereby maintaining a high barrier resistance comparable to nonstressed cells. In docking analyses exploring the putative interaction with the tyrosine kinase EGFR, these novel modulators of barrier tightness showed very similar values compared to the known tyrosine kinase inhibitor genistein. Both biochanin A and prunetin were also identified as potent reducers of NF-κB and ERK activation, zonula occludens 1 tyrosine phosphorylation, and metalloproteinase-mediated shedding activity, which may account for the barrier-improving ability of these isoflavones.

Neonicotinoid insecticides severely affect honey bee queens

Queen health is crucial to colony survival of social bees. Recently, queen failure has been proposed to be a major driver of managed honey bee colony losses, yet few data exist concerning effects of environmental stressors on queens. Here we demonstrate for the first time that exposure to field realistic concentrations of neonicotinoid pesticides during development can severely affect queens of western honey bees (Apis mellifera). In pesticide-exposed queens, reproductive anatomy (ovaries) and physiology (spermathecal-stored sperm quality and quantity), rather than flight behaviour, were compromised and likely corresponded to reduced queen success (alive and producing worker offspring). This study highlights the detriments of neonicotinoids to queens of environmentally and economically important social bees, and further strengthens the need for stringent risk assessments to safeguard biodiversity and ecosystem services that are vulnerable to these substances.

Immunotoxic effects of environmental toxicants in fish - how to assess them?

Numerous environmental chemicals, both long-known toxicants such as persistent organic pollutants as well as emerging contaminants such as pharmaceuticals, are known to modulate immune parameters of wildlife species, what can have adverse consequences for the fitness of individuals including their capability to resist pathogen infections. Despite frequent field observations of impaired immunocompetence and increased disease incidence in contaminant-exposed wildlife populations, the potential relevance of immunotoxic effects for the ecological impact of chemicals is rarely considered in ecotoxicological risk assessment. A limiting factor in the assessment of immunotoxic effects might be the complexity of the immune system what makes it difficult (1) to select appropriate exposure and effect parameters out of the many immune parameters which could be measured, and (2) to evaluate the significance of the selected parameters for the overall fitness and immunocompetence of the organism. Here, we present - on the example of teleost fishes - a brief discussion of how to assess chemical impact on the immune system using parameters at different levels of complexity and integration: immune mediators, humoral immune effectors, cellular immune defenses, macroscopical and microscopical responses of lymphoid tissues and organs, and host resistance to pathogens. Importantly, adverse effects of chemicals on immunocompetence may be detectable only after immune system activation, e.g., after pathogen challenge, but not in the resting immune system of non-infected fish. Current limitations to further development and implementation of immunotoxicity assays and parameters in ecotoxicological risk assessment are not primarily due to technological constraints, but are related from insufficient knowledge of (1) possible modes of action in the immune system, (2) the importance of intra- and inter-species immune system variability for the response against chemical stressors, and (3) deficits in conceptual and mechanistic assessment of combination effects of chemicals and pathogens.

Assessing the impact of multiple stressors on aquatic biota: the receptor's side matters.

Aquatic ecosystems are confronted with multiple stress factors. Current approaches to assess the risk of anthropogenic stressors to aquatic ecosystems are developed for single stressors and determine stressor effects primarily as a function of stressor properties. The cumulative impact of several stressors, however, may differ markedly from the impact of the single stressors and can result in nonlinear effects and ecological surprises. To meet the challenge of diagnosing and predicting multiple stressor impacts, assessment strategies should focus on properties of the biological receptors rather than on stressor properties. This change of paradigm is required because (i) multiple stressors affect multiple biological targets at multiple organizational levels, (ii) biological receptors differ in their sensitivities, vulnerabilities, and response dynamics to the individual stressors, and (iii) biological receptors function as networks, so that actions of stressors at disparate sites within the network can lead via indirect or cascading effects, to unexpected outcomes.

Bedouin in the Negev and Environmental Studies: Current and Future Research Prospects

Environmental aspects are increasingly being integrated in Negev Bedouin studies by both, NGO activists and scholars. We will present these recent works and discuss new concepts and methodologies of environmental studies with potential relevance in the field of Negev Bedouin studies. We will then identify research areas where environmental and development approaches converge or diverge with mainstream social sciences on this specific field of research. While most of the Bedouin population in southern Israel lives in urban centers in the Northern Negev, a large part of Bedouin people live in unrecognized clusters of houses in remote areas. Extensive livestock rearing is an important source of livelihood at least for non-urbanized Bedouin, the latter forming the lowest economic strata of the Israeli spectrum of incomes. Numerous stressors affect this Bedouin community enduring uncertain livelihood and access to land. The erratic precipitations from year to year and long-term changes in precipitation trends are a source of great uncertainty. With a significant price increase for feeding supplements to compensate for dry years, livestock rearing has become a harsher source of livelihood. Land scarcity for grazing adds to the difficulty in ensuring enough income for living. Studies in the last 15 years have described several livelihood strategies based on a livestock rearing semi-nomadic economy in the Negev. A number of other analyses have shown how Bedouin herders and governmental agencies have found agreements at the advantage of both, the agencies and the herders. New concepts such as transformability, resilience and adaptation strategies are important tools to analyze the capacity of vulnerable communities to cope with an ever increasing livelihood uncertainty. Such research concepts can assist in better understanding how Bedouin herders in the Negev may adapt to climate and political risks.

Effects, but no interactions, of ubiquitous pesticide and parasite stressors on honey bee (Apis mellifera) lifespan and behaviour in a colony environment

Interactions between pesticides and parasites are believed to be responsible for increased mortality of honey bee (Apis mellifera) colonies in the northern hemisphere. Previous efforts have employed experimental approaches using small groups under laboratory conditions to investigate influence of these stressors on honey bee physiology and behaviour, although both the colony level and field conditions play a key role for eusocial honey bees. Here, we challenged honey bee workers under in vivo colony conditions with sublethal doses of the neonicotinoid thiacloprid, the miticide tau-fluvalinate and the endoparasite Nosema ceranae, to investigate potential effects on longevity and behaviour using observation hives. In contrast to previous laboratory studies, our results do not suggest interactions among stressors, but rather lone effects of pesticides and the parasite on mortality and behaviour, respectively. These effects appear to be weak due to different outcomes at the two study sites, thereby suggesting that the role of thiacloprid, tau-fluvalinate and N. ceranae and interactions among them may have been overemphasized. In the future, investigations into the effects of honey bee stressors should prioritize the use of colonies maintained under a variety of environmental conditions in order to obtain more biologically relevant data.