Biology subjects

Common, J.

Publications and source records attributed to Common, J..

4 recordsLinked to original sources

bioRxiv2024

Climatic predictors of prominent honey bee (Apis mellifera) disease agents: Varroa destructor, Melissococcus plutonius, and Vairimorpha spp.

Improving our understanding of how climate influences honey bee parasites and pathogens is critical as weather patterns continue to shift under climate change. While the prevalence of diseases vary according to regional and seasonal patterns, the influence of specific climatic predictors has rarely been formally assessed. To address this gap, we analyzed how occurrence and intensity of three prominent honey bee disease agents (Varroa destructor [-] hereon Varroa [-] Melissococcus plutonius, and Vairimorpha spp.) varied according to regional, temporal, and climatic factors in honey bee colonies across five Canadian provinces. We found strong regional effects for all disease agents, with consistently high Varroa intensity and infestation probabilities and high M. plutonius infection probabilities in British Columbia, and year-dependent regional patterns of Vairimorpha spp. spore counts. Increasing wind speed and precipitation were linked to lower Varroa infestation probabilities, whereas warmer temperatures were linked to higher infestation probabilities. Analysis of an independent dataset shows that these trends for Varroa are consistent within a similar date range, but temperature is the strongest climatic predictor of season-long patterns. Vairimorpha spp. intensity decreased over the course of the summer, with the lowest spore counts found at later dates when temperatures were warm. Vairimorpha spp. intensity increased with wind speed and precipitation, consistent with inclement weather limiting defecation flights. Probability of M. plutonius infection generally increased across the spring and summer, and was also positively associated with inclement weather. These data contribute to building a larger dataset of honey bee disease agent occurrence that is needed in order to predict how epidemiology may change in our future climate.

molecular biology↗

bioRxiv2024

Higher prevalence of sacbrood virus in highbush blueberry pollination units

Highbush blueberry pollination depends on managed honey bees (Apis mellifera) for adequate fruit set; however, beekeepers have raised concerns about poor health of colonies after pollinating this crop. Postulated causes include agrochemical exposure, nutritional deficits, and interactions with parasites and pathogens, particularly Melisococcus plutonius(the causal agent of European foulbrood disease), but other pathogens could be involved. To broadly investigate common honey bee pathogens in relation to blueberry pollination, we sampled adult honey bees from colonies at time points corresponding to before (t1), during (t2), at the end (t3), and after (t4) highbush blueberry pollination in British Columbia (BC), Canada, across two years (2020 and 2021). Nine viruses as well as M. plutonius, Vairimorpha ceranae and V. apis (formerly Nosema ceranae and N. apis) were detected by PCR and microscopy and compared among colonies located near and far from blueberry fields. We found a significant interactive effect of time and blueberry proximity on the multivariate pathogen community, mainly due to differences at t4 (corresponding to roughly six weeks after the beginning of the pollination period). Post-hoc comparisons of pathogens in near and far groups at t4 showed that detections of sacbrood virus (SBV), which was significantly higher in the exposed group, was the primary driver. The association of SBV with highbush blueberry pollination may be contributing to the health decline that beekeepers observe after pollinating this crop, likely in combination with other factors.

zoology↗

bioRxiv2024

Life stage impact on the human skin ecosystem: lipids and the microbial community

While research into gut-microbe interactions is common and advanced, with multiple defined impacts on human health, studies exploring the significance of skin-microbe interactions remain underrepresented. Skin is the largest human organ, has a vast surface area, and is inhabited by a plethora of microorganisms which metabolise sebaceous lipids. Sebaceous free fatty acids are metabolized into bioactive lipid mediators with immune-modulatory properties by skin-resident microbes, including Malassezia. Intriguingly, many of the same lipid mediators are also found on human skin, implying these compounds may have microbial or mixed microbial/human origin. To support this hypothesis, we isolated lipids and microbial DNA from the skin of prepubescent, adult, pre- and post-menopausal volunteers and performed correlational analyses using skin lipidomics and metagenomics to compare lipid mediator profiles and microbiome compositions on skin with either low or high sebaceous gland activity. We found that specific microbial taxonomies were positively and negatively correlated with skin lipid mediator species with high statistical significance. 2D in vitro co-cultures with Malassezia and keratinocytes also directly linked the production of specific lipid mediators, detected on healthy human skin, to secretion of immuno-stimulatory cytokines. Together, these findings further support the hypothesis that microbial-derived skin lipid mediators influence healthy skin homeostasis and skin disease development and progression, thereby spotlighting the relevance of the skin microbiomes footprint on human health.

microbiology↗

bioRxiv2019

Host resistance diversity protects susceptible genotypes by restricting pathogen spread and evolution

Diversity in host resistance often associates with reduced pathogen spread. This may result from ecological and evolutionary processes, likely with feedback between them. Theory and experiments on bacteria-phage interactions have shown that genetic diversity of the bacterial adaptive immune system can limit phage evolution to overcome resistance. Using the CRISPR-Cas bacterial immune system and lytic phage, we engineered a host-pathogen system where each bacterial host genotype could be infected by only one phage genotype. With this model system, we explored how CRISPR diversity impacts the spread of phage when they can overcome a resistance allele, how immune diversity affects the evolution of the phage to increase its host range, and if there was feedback between these processes. We show that increasing CRISPR diversity benefits susceptible bacteria via a dilution effect, which limits the spread of the phage. We suggest that this ecological effect impacts the evolution of novel phage genotypes, which then feeds back into phage population dynamics.

evolutionary biology↗