Attempts to Reproduce Vacuolar Myelinopathy in Domestic Swine and Chickens

Abstract

Avian vacuolar myelinopathy (AVM) was first recognized as a cause of bald eagle (Haliaeetus leucocephalus) mortality in 1994 in Arkansas (USA) and has since caused over 90 bald eagle and numerous American coot (Fulica americana) mortalities in five southeastern states. The cause of AVM remains undetermined but is suspected to be a biotoxin. Naturally occurring AVM has been limited to wild waterbirds, raptors, and one species of shorebird, and has been reproduced experimentally in red-tailed hawks (Buteo jamaicensis). In this study, chickens and swine were evaluated for susceptibility to vacuolar myelinopathy with the intent of developing animal models for research and to identify specific tissues in affected coots that contain the causative agent. Additionally, submerged, aquatic vegetation, primarily hydrilla (Hydrilla verticillata), and associated material collected from a reservoir during an AVM outbreak was fed to chickens in an effort to reproduce the disease. In two separate experiments, six 4-wk-old leghorn chickens and ten 5-wk-old leghorn chickens were fed coot tissues. In a third experiment, five 3-mo-old domestic swine and one red-tailed hawk, serving as a positive control, were fed coot tissues. In these experiments, treatment animals received tissues (brain, fat, intestinal tract, kidney, liver, and/or muscle) from coots with AVM lesions collected at a lake during an AVM outbreak. Negative control chickens and one pig received tissues from coots without AVM lesions that had been collected at a lake where AVM has never been documented. In a fourth experiment, eight 3-wk-old leghorn chickens were fed aquatic vegetation material. Four chickens received material from the same lake from which coots with AVM lesions were collected for the previous experiments, and four control chickens were fed material from the lake where AVM has never been documented. Blood was collected and physical and neurologic exams were conducted on animals before and once per week during the trials. All animals were sacrificed and necropsies were performed on Day 29 of feeding, with the exception of one treated chicken that was sacrificed and necropsied on Day 15 of feeding. Microscopic lesions of vacuolar myelinopathy were present in the red-tailed hawk and five chickens that received a mixture of all tissues and two chickens that received only gastrointestinal tissues of coots with AVM lesions. Three of four treated chickens in the aquatic vegetation trial developed vacuolar lesions. None of four treatment pigs or any of the negative control animals developed vacuolar lesions. Chickens are susceptible to AVM and may serve as a useful animal model for future studies. Swine may be refractory to AVM or not affected by AVM at the same dose as are chickens and red-tailed hawks. The causative agent of AVM in affected coots is associated with the gastrointestinal tissues. Furthermore, AVM can be reproduced in chickens via ingestion of aquatic vegetation and associated materials collected from a lake during an AVM outbreak. T...

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).…”

“…Previous AVM feeding studies utilizing two to five chickens per treatment validated them as an appropriate laboratory surrogate for wild birds (Lewis-Weis et al 2004). Chicks in both trials were randomly divided into control (n¼5) and treatment (n¼5) groups and housed in individual isolation units (Horsfal units) to prevent exposure to exogenous toxicants or stressors and to monitor diet consumption.…”

“…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.…”

“…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). Because the AVM toxin is uncharacterized, an avian bioassay is the only available method to illustrate toxicity of SAV material containing A. hydrillicola.…”