Investigation of the link between avian vacuolar myelinopathy and a novel species of cyanobacteria through laboratory feeding trials.

Avian vacuolar myelinopathy (AVM) is a neurologic disease affecting Bald Eagles (Haliaeetus leucocephalus), American Coots (Fulica americana), and other birds in the southeastern United States. The cause of the disease has not yet been determined, although it is generally thought to be a natural toxin. Previous studies have linked AVM to aquatic vegetation, and the current working hypothesis is that a species of cyanobacteria growing epiphytically on that vegetation is producing a toxin that causes AVM. Surveys of epiphytic communities have identified a novel species of cyanobacteria in the order Stigonematales as the most likely suspect. The purpose of this study was to further examine the relationship between the suspect Stigonematales species and induction of AVM, by using animal feeding trials. Adult Mallards and domestic chickens were fed aquatic vegetation from two study sites containing the suspect cyanobacterial epiphyte, as well as a control site that did not contain the Stigonematales species. Two trials were conducted. The first trial used vegetation collected during mid-October 2003, and the second trial used vegetation collected during November and December 2003. Neither treatment nor control birds in the first trial developed AVM lesions. Ten of 12 treatment Mallards in the second trial were diagnosed with AVM, and control birds were not affected. This study provides further evidence that the novel Stigonematales species may be involved with AVM induction, or at the least it is a good predictor of AVM toxin presence in a system. The results also demonstrate the seasonal nature of AVM events.

Establishing a food-chain link between aquatic plant material and avian vacuolar myelinopathy in mallards (Anas platyrhynchos).

Avian vacuolar myelinopathy (AVM) is a neurologic disease primarily affecting bald eagles (Haliaeetus leucocephalus) and American coots (Fulica americana). The disease was first characterized in bald eagles in Arkansas in 1994 and then in American coots in 1996. To date, AVM has been confirmed in six additional avian species. Attempts to identify the etiology of AVM have been unsuccessful to date. The objective of this study was to evaluate dermal and oral routes of exposure of birds to hydrilla (Hydrilla verticillata) and associated materials to evaluate their ability to induce AVM. Mallards (Anas platyrhynchos) were used in all trials; bobwhite quail (Colinus virginianus) also were used in one fresh hydrilla material exposure trial. Five trials were conducted, including two fresh hydrilla material exposure trials, two cyanobacteria exposure trials, and a frozen hydrilla material exposure trial. The cyanobacteria exposure trials and frozen hydrilla material trial involved gavaging mallards with either Pseudanabaena catenata (live culture), Hapalosiphon fontinalis, or frozen hydrilla material with both cyanobacteria species present. With the exception of one fresh hydrilla exposure trial, results were negative or inconclusive. In the 2002 hydrilla material exposure trial, six of nine treated ducks had histologic lesions of AVM. This established the first cause-effect link between aquatic vegetation and AVM and provided evidence supporting an aquatic source for the causal agent.

Avian vacuolar myelinopathy linked to exotic aquatic plants and a novel cyanobacterial species.

Invasions of exotic species have created environmental havoc through competition and displacement of native plants and animals. The introduction of hydrilla (Hydrilla verticillata) into the United States in the 1960s has been detrimental to navigation, power generation, water intake, and water quality (McCann et al., 1996). Our field surveys and feeding studies have now implicated exotic hydrilla and associated epiphytic cyanobacterial species as a link to avian vacuolar myelinopathy (AVM), an emerging avian disease affecting herbivorous waterbirds and their avian predators. AVM, first reported in 1994, has caused the death of at least 100 bald eagles (Haliaeetus leucocephalus) and thousands of American coots (Fulica americana) at 11 sites from Texas to North Carolina (Thomas et al., 1998; Rocke et al., 2002). Our working hypothesis is that the agent of this disease is an uncharacterized neurotoxin produced by a novel cyanobacterial epiphyte of the order Stigonematales. This undescribed species covers up to 95% of the surface area of leaves in reservoirs where bird deaths have occurred from the disease. In addition, this species is rare or not found on hydrilla collected at sites where AVM disease has not been diagnosed. Laboratory feeding trials and a sentinel bird study using naturally occurring blooms of cyanobacteria on hydrilla leaves and farm-raised mallard ducks (Anas platyrhynchos) induced the disease experimentally. Since 1994 AVM has been diagnosed in additional sites from Texas to North Carolina. Specific site characteristics that produce the disjunct distribution of AVM are unknown, but it is probable that the incidence of this disease will increase with the introduction of hydrilla and associated cyanobacterial species into additional ponds, lakes, and reservoirs.