The Great Salt Lake (GSL) is a significant stopover point and breeding ground for millions of migratory birds along the Pacific Flyway, yet it is also the site of recurring, devastating mass mortality events. These die-offs are the result of specific pathogens and environmental stressors that thrive in the lake’s unique and increasingly compromised ecosystem. Understanding the causes requires examining the lake’s primary biological threat and the environmental changes that fuel its spread.
The Dominant Cause: Avian Botulism
The single most frequent and impactful biological cause of mass bird deaths at the GSL is Avian Botulism. This disease is caused by a potent neurotoxin produced by the bacterium Clostridium botulinum. The bacterial spores are common in wetland sediments, remaining dormant until specific conditions allow them to germinate and multiply.
The toxin causes a progressive, paralytic syndrome in affected birds. Paralysis often affects the legs and wings, making it difficult for the bird to walk or fly. Eventually, the paralysis extends to the neck muscles, resulting in the characteristic “limberneck” posture, which often leads to drowning or death from starvation. The bacteria thrive in warm temperatures, decaying organic matter, and anaerobic conditions (very little or no oxygen).
The disease spreads rapidly through the “carcass-maggot” cycle. When an animal dies and its tissue decays, Clostridium botulinum rapidly colonizes the carcass and produces large amounts of neurotoxin. Fly maggots that feed on this infected tissue concentrate the toxin within their bodies. Healthy waterfowl and shorebirds ingest these toxin-laced maggots, quickly becoming paralyzed and perpetuating the cycle of death. A single major outbreak can kill tens of thousands of birds, with some historical events estimated to have killed over 500,000 waterfowl.
How the Lake’s Condition Fuels Mortality Events
The physical and chemical condition of the Great Salt Lake is the primary catalyst that transforms the persistent bacterium into a widespread epidemic. Persistent drought and water diversion have caused the lake’s water levels to drop to historic lows. This reduced water volume concentrates nutrients and increases the lake’s overall temperature, creating an incubator for botulism outbreaks.
Shallow, stagnant water heats up quickly during summer, and the lack of fresh inflow reduces dissolved oxygen levels. These warm, oxygen-deprived (anoxic) environments allow the Clostridium botulinum spores to germinate and produce their paralyzing toxin. The low-water crisis also expands exposed mudflats and shallow areas, which concentrate birds in smaller foraging zones.
This concentration of birds in a degraded habitat increases stress and accelerates the spread of the disease. Furthermore, low water levels interrupt the lake’s complex food web, including the brine shrimp and brine flies that millions of birds rely on. When food sources are scarce, birds become physically weaker and more susceptible to disease, making them less likely to survive the neurotoxin.
Secondary Threats and Environmental Toxins
Beyond the immediate threat of Avian Botulism, low water levels expose the ecosystem to hazards from long-dormant chemical contamination. The drying lakebed contains sediments rich in heavy metals like mercury, arsenic, and selenium, deposited over decades from natural sources and industrial activity. As the lake recedes, these metals become available and pose a threat to foraging birds.
These metals enter the food chain and become concentrated through bioaccumulation and biomagnification. Tiny organisms and invertebrates, such as brine flies and brine shrimp, ingest the contaminants from the sediment and water. When birds consume large quantities of this contaminated prey, the toxins build up in their tissues at toxic levels.
Mercury is a known concern at the GSL. Exposure to these heavy metals can cause neurological damage, reproductive failure, and impaired growth in birds, weakening their overall health. While these toxins may not cause the massive, acute die-offs seen with botulism, they represent a significant, chronic threat that compromises the long-term viability of the avian population.