Date of Award

Fall 2024

Project Type

Dissertation

Program or Major

Biological Sciences

Degree Name

Doctor of Philosophy

First Advisor

James F. Haney

Second Advisor

Nathan Furey

Third Advisor

Mark Pokras

Abstract

Toxins produced by cyanobacteria (hereafter, cyanotoxins) are among the most lethal known biotoxins. Cyanotoxin exposure is assumed to occur mainly through direct contact with surface-bloom-forming cyanobacteria that are most commonly observed in warm, nutrient-rich lakes. However, recent observations of cyanotoxin accumulation in the Greater Yellowstone Ecosystem (GYE), an area where cyanobacteria blooms are rarely observed, have raised concerns over wildlife health in this highly protected region. In response, we sampled twelve clear-water lakes in the GYE to identify potential sources of cyanotoxins (particularly the neurotoxin beta-methylamino-L-alanine, BMAA), exposure routes, and health risks.Despite nutrient limitations and cool water temperatures, the sampled lakes supported dense communities of picocyanobacteria, littoral periphyton, and, in some cases, benthic biofilms. These cyanobacteria-containing communities produced at least three cyanotoxins, including BMAA, microcystins (MCs), and anatoxin-a (ATX). Cyanobacteria biomass (represented by phycocyanin and phycoerythrin concentrations) and nutrient limitation (represented by carbon-to-nitrogen ratios in microphytes) were the primary determinants of BMAA levels in lake waters. Due to high cyanobacterial toxicity and non-blooming (not visible at the lake surface) cyanobacteria biomass, clear-water lakes in the GYE produced BMAA at levels (> 100 μg L-1) comparable to those found under severe cyanobacteria bloom conditions. Consequently, several GYE lakes warrant additional cyanobacteria monitoring and potential management action despite their seemingly pristine appearance. Contrary to expectations, grazing by zooplankton and macroinvertebrates had little direct effect on the toxicity or abundance of cyanobacteria. Instead, top-down control by grazers altered the quality of microphyte food items and indirectly facilitated energy transfer through pelagic pathways while simultaneously dampening benthic and littoral energy flow. Nonetheless, these shifts in food web composition and structure had only minor effects on cyanotoxin accumulation across the food web. BMAA biomagnified between cyanobacteria and invertebrate grazers but biodiluted between invertebrates and vertebrate predators in both lake types (containing fish and fishless). Despite their previous classification as non-biomagnifying toxins, anatoxin-a (ATX) and microcystins (MCs) showed similar potential for extreme biomagnification and biodilution within aquatic food webs. Although biomagnification did not occur consistently throughout lake food chains, models suggest that dietary intake was the primary pathway of BMAA exposure for predatory vertebrates in the GYE. BMAA uptake through the gills significantly increased modeled exposure in some fish. Meanwhile, models suggest that the inhalation of aerosols, contact with soils, and maternal transfer contributed little to overall exposure in the sampled vertebrates but could be important exposure pathways in other habitats or for other species. Based on the toxin concentrations observed in the GYE, exposure to BMAA, ATX, and MCs is expected to exceed provisional intake thresholds for various lake vertebrates, raising concerns about wildlife health in this region. However, because intake thresholds are still provisional, the significance of this exposure and the specific health risks remain unknown. These results emphasize a need to improve and expand monitoring efforts and to identify the specific health effects associated with acute and long-term exposure to BMAA and other cyanotoxins. This need is particularly pressing in cool, clear-water lakes and other vulnerable systems that are traditionally overlooked in current monitoring efforts.

Available for download on Friday, January 23, 2026

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