Establishing a Food-Chain Link Between Aquatic Plant Material and Avian Vacuolar Myelinopathy in Mallards (Anas Platyrhynchos)

Abstract

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.

Aetokthonos hydrillicola gen. et sp. nov.: Epiphytic cyanobacteria on invasive aquatic plants implicated in Avian Vacuolar Myelinopathy

“…These dense, invasive aquatic macrophyte beds provide ideal substrate for attachment by epiphytic cyanobacteria capable of toxin production and should be considered when evaluating risk of harmful algae in water supply lakes and reservoirs (Wilde et al 2005, Mohamed & Al-Shehri 2010. Feeding trials and field surveys support the hypothesis that birds ingest an unknown neurotoxin produced by this novel epiphytic cyanobacterial species colonizing the aquatic plants (Birrenkott et al 2004, Wilde et al 2005, Wiley et al 2009, Haynie et al 2013. Identification of this cyanobacterial species is critical in order to advance neurotoxin isolation and characterization work that is currently underway.…”

ALTERNATE FOOD-CHAIN TRANSFER OF THE TOXIN LINKED TO AVIAN VACUOLAR MYELINOPATHY AND IMPLICATIONS FOR THE ENDANGERED FLORIDA SNAIL KITE (ROSTRHAMUS SOCIABILIS)

“…Species that specialize on dietary items that contain high levels of AVM toxin are most at risk (e.g., coots [hydrilla], and eagles [coots]; Birrenkott et al 2004;Lewis-Weis et al 2004). The density of A. hydrillicola colonies observed on Toho hydrilla is comparable to those in AVM reservoirs in South Carolina and Georgia (Wilde et al 2005).…”

“…Laboratory studies have confirmed that AVM toxin can be transferred up the food chain from herbivorous waterbirds to predatory raptors Birrenkott et al 2004;Lewis-Weis et al 2004). We predicted that Snail Kites would be susceptible to the toxin that causes AVM similar to Bald Eagles, Red-tailed Hawks (Buteo jamaicensis), and Great Horned Owls (Bubo virginianus) that developed AVM lesions after consuming prey from an AVM site (Lewis-Weis et al 2004).…”

“…Treatment diet measurements were based on previous feeding studies ( LewisWeis et al 2004;Wiley et al 2009). This initial trial was necessary to ensure the AVM toxin was present in the vegetation collection before proceeding with the snail feeding trial (Birrenkott et al 2004;Wiley et al 2007). …”

“…Aetokthonos hydrillicola dominates the epiphyte community on the leaves of SAV in AVM sites but is rare or not present in sites where AVM deaths have not occurred (Wilde et al 2005Williams et al 2007). Feeding studies have implicated food chain transfer (via ingestion of the gastrointestinal tract of diseased birds) of a toxin produced by a cyanobacterium associated with submerged aquatic vegetation growing in waterbodies where AVM-positive birds were previously diagnosed Birrenkott et al 2004;Lewis-Weis et al 2004;Rocke et al 2005;Wilde et al 2005Wilde et al , 2014. Thus, the working hypothesis of all ongoing AVM investigations is that waterbirds develop AVM by ingesting SAV and A. hydrillicola either directly or via predation on other birds that have recently fed on this material.…”