Areas of concern (AOCs) around the Great Lakes are characterized by historic and ongoing problems with microbial water quality, leading to beneficial use impairments (BUIs) such as beach postings and closures. In this study, we assessed river and beach sites within the Rouge River watershed, associated stormwater outfalls, and at Rouge Beach. The concentrations of as well as human- and gull-specific qPCR microbial source tracking (MST) markers were assessed at all sites. A preliminary comparison of digital PCR (dPCR) methodologies for both MST markers was conducted regarding sensitivity and specificity. Within the watershed, the outfalls were found to be a prominent source of human fecal contamination, with two outfalls particularly affected by sewage cross-connections. However, the occurrence of human fecal contamination along Rouge Beach and in the lower portions of the watershed was largely dependent on rain events. Gull fecal contamination was the predominant source of contamination at the beach, particularly during dry weather. The multiplex human/gull dPCR methodology used in this study tended to be more sensitive than the individual quantitative PCR (qPCR) assays, with only a slight decrease in specificity. Both dPCR and qPCR methodologies identified the same predominance of human and gull markers in stormwater and beach locations, respectively; however, the dPCR multiplex assay was more sensitive and capable of detecting fecal contamination that was undetected by qPCR assays. These results demonstrate the dPCR assay used in this study could be a viable tool for MST studies to increase the ability to identify low levels of fecal contamination. Fecal contamination of recreational water poses a persistent and ongoing problem, particularly in areas of concern around the Great Lakes. The identification of the source(s) of fecal contamination is essential for safeguarding public health as well as guiding remediation efforts; however, fecal contamination may frequently be present at low levels and remain undetectable by certain methodologies. In this study, we utilized microbial source tracking techniques using both quantitative and digital PCR assays to identify sources of contamination. Our results indicated high levels of human fecal contamination within stormwater outfalls, while lower levels were observed throughout the watershed. Additionally, high levels of gull fecal contamination were detected at Rouge Beach, particularly during drier sampling events. Furthermore, our results indicated an increased sensitivity of the digital PCR assay to detect both human and gull contamination, suggesting it could be a viable tool for future microbial source tracking studies.

Multifactorial diseases are characterized by inter-individual variation in etiology, age of onset, and penetrance. These diseases tend to be relatively common and arise from the combined action of genetic and environmental factors; however, parsing the convoluted mechanisms underlying these gene-by-environment interactions presents a significant challenge to their study and management. For neurodegenerative disorders, resolving this challenge is imperative, given the enormous health and societal burdens they impose. The mechanisms by which genetic and environmental effects may act in concert to destabilize homeostasis and elevate risk has become a major research focus in the study of common disease. Emphasis is further being placed on determining the extent to which a unifying biological principle may account for the progressively diminishing capacity of a system to buffer disease phenotypes, as risk for disease increases. Data emerging from studies of common, neurodegenerative diseases are providing insights to pragmatically connect mechanisms of genetic and environmental risk that previously seemed disparate. In this review, we discuss evidence positing inflammation as a unifying biological principle of homeostatic destabilization affecting the risk, onset, and progression of neurodegenerative diseases. Specifically, we discuss how genetic variation associated with Alzheimer disease and Parkinson disease may contribute to pro-inflammatory responses, how such underlying predisposition may be exacerbated by environmental insults, and how this common theme is being leveraged in the ongoing search for effective therapeutic interventions.

Immune defences often trade off with other life-history components. Within species, optimal allocation to immunity may differ between the sexes or between alternative life-history strategies. White-throated sparrows () are unusual in having two discrete plumage morphs, white-striped and tan-striped. Within each sex, white-striped individuals are more aggressive and provide less parental care than tan-striped individuals. We extended immunocompetence handicap models, which predict sex differences in immunity and parasitism, to hypothesize that infection susceptibility should be greater in white-striped than tan-striped birds. We inoculated birds of both morphs with malarial parasites. Contrary to our prediction, among birds that became infected, parasite loads were higher in tan-striped than white-striped individuals and did not differ between the sexes. Circulating androgen levels did not differ between morphs but were higher in males than females. Our findings are not consistent with androgen-mediated immunosuppression. Instead, morph differences in immunity could reflect social interactions or life-history-related differences in risk of injury, and/or genetic factors. Although plumage and behavioural morphs of white-throated sparrow may differ in disease resistance, these differences do not parallel sex differences that have been reported in animals, and do not appear to be mediated by differences in androgen levels.

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