David Linz

When cyanobacterial phytoplankton form harmful cyanobacterial blooms (HCBs), the toxins they produce threaten freshwater ecosystems. Hydrogen peroxide is often used to control HCBs, but it is broadly toxic and dangerous to handle. Previously, we demonstrated that glucose addition to lake water could suppress the abundance of cyanobacteria. In this study, glucose was compared to hydrogen peroxide for the treatment of cyanobacterial phytoplankton communities. The six-week study was conducted in the large mesocosms facility at Grand Valley State University’s Annis Water Resources Institute in Michigan. To 1000 L of Muskegon Lake water, glucose was added at either 150 mg or 30 mg glucose/L. Hydrogen peroxide was added at 3 mg/L to two 1000 L mesocosms. And two mesocosms were left untreated as controls. Triplicate 100 mL samples were collected weekly from each mesocosm, which were then filtered and frozen at −80 °C for 16S rRNA amplicon sequencing. The 16S rRNA amplicon sequencing results revealed that hydrogen peroxide treatment quickly reduced the relative abundance of the cyanobacteria compared to the control mesocosms, but the cyanobacteria population returned over the course of the 6-week study. On the other hand, both glucose concentrations caused a rapid proliferation of multiple low abundance proteobacterial and bacteroidotal taxa resulting in notable increases in taxonomic richness over the duration of the study and reducing the relative abundance of cyanobacteria. Although hydrogen peroxide quickly suppressed the cyanobacteria, the population later returned to near starting levels. The glucose suppressed the cyanobacterial phytoplankton apparently by promoting competitive heterotrophic bacteria.

Populations of resident, non-migratory Canada geese are rapidly increasing. Canada geese are known to transmit viral and bacterial diseases, posing a possible threat to human health. The most prevalent pathogens vectored by geese are Campylobacter species, yet the current understanding of the identity and virulence of these pathogens is limited. In our previous study, we observed a high prevalence of Campylobacter spp. in the Banklick Creek wetland—a constructed treatment wetland (CTW) located in northern KY (USA) used to understand sources of fecal contamination originating from humans and waterfowl frequenting the area. To identify the types of Campylobacter spp. found contaminating the CTW, we performed genetic analyses of Campylobacter 16s ribosomal RNA amplified from CTW water samples and collected fecal material from birds frequenting those areas. Our results showed a high occurrence of a Campylobacter canadensis-like clade from the sampling sites. Whole-genome sequence analyses of an isolate from Canada goose fecal material, called MG1, were used to confirm the identity of the CTW isolates. Further, we examined the phylogenomic position, virulence gene content, and antimicrobial resistance gene profile of MG1. Lastly, we developed an MG1-specific real-time PCR assay and confirmed the presence of MG1 in Canada goose fecal samples surrounding the CTW. Our findings reveal that the Canada goose-vectored Campylobacter sp. MG1 is a novel isolate compared to C. canadensis that possesses possible zoonotic potential, which may be of human health concern.

To mitigate harmful cyanobacterial blooms (HCBs), toxic algicides have been used, but alternative methods of HCB prevention are needed. Our goal was to test the prophylactic addition of glucose to inhibit HCB development, using Microcystis and the toxin microcystin as the HCB model. Water samples were collected weekly, from 4 June to 2 July, from Harsha Lake in southwestern Ohio during the 2021 algal bloom season. From each weekly sample, a 25 mL aliquot was frozen for a 16S rRNA gene sequencing analysis. Then, 200 mL of Harsha Lake water was added to each of the three culture flasks, and glucose was added to create concentrations of 0 mM (control), 1.39 mM, or 13.9 mM glucose, respectively. The microcystin concentration in each flask was measured after 1 and 2 weeks of incubation. The results showed an 80 to 90% reduction in microcystin concentrations in glucose-treated water compared to the control. At the end of the second week of incubation, a 25 mL sample was also obtained from each of the culture flasks for molecular analysis, including a 16S rRNA gene sequencing and qPCR-based quantification of Microcystis target genes. Based on these analyses, the glucose-treated water contained significantly lower Microcystis and microcystin producing gene (mcy) copy numbers than the control. The 16S rRNA sequencing analysis also revealed that Cyanobacteria and Proteobacteria were initially the most abundant bacterial phyla in the Harsha Lake water, but as the summer progressed, Cyanobacteria became the dominant phyla. However, in the glucose-treated water, the Cyanobacteria decreased and the Proteobacteria increased in weekly abundance compared to the control. This glucose-induced proteobacterial increase in abundance was driven primarily by increases in two distinct families of Proteobacteria: Devosiaceae and Rhizobiaceae. In conclusion, the prophylactic addition of glucose to Harsha Lake water samples reduced Cyanobacteria’s relative abundance, Microcystis numbers and microcystin concentrations and increased the relative abundance of Proteobacteria compared to the control.