Abstract

Over the course of five weeks in early 2011, 1247 Canada geese (Branta canadensis) died on a private estate in New Castle County, Delaware. Geese were found dead or dying, with live birds reported to be "wobbly" prior to death. No secondary mortalities were observed despite predation on carcasses by foxes, hawks, and other scavengers. Resident ducks that were fed the same whole corn on site were not affected; however, the geese also foraged elsewhere during the daytime. Differential diagnoses included various toxicants (road salt, mycotoxins, anticoagulant rodenticides, pesticides, lead, urea) and infectious diseases (avian influenza, Newcastle disease, Salmonella). Among six birds transported to a rehabilitation center for care, one died in transit, and another died within 2 hours of admission. Six hours after admission, two more birds seizured and regurgitated and then died overnight. The two surviving birds eventually improved with extensive supportive care.

Dead birds were examined by three independent laboratories (University of Pennsylvania, University of Delaware, and USGS National Wildlife Health Center). Primary findings included severe, acute, diffuse tubular necrosis and obstructive cast formation; elevated serum iron, phosphorus, and potassium levels; elevated kidney calcium levels; normal sodium levels. Diagnostic testing for pesticides (including avicides), ethylene glycol, lead, Salmonella, avian influenza, and Newcastle disease was negative. With many other possible differentials ruled out and an abrupt end to the observed mortalities, a feed-associated toxicant was suspected. Gastrointestinal contents, corn being fed on-site (feed corn), and corn from a nearby field (field corn) were all tested for mycotoxins; however, it is not believed that the geese were actively feeding on the field corn. All samples were positive for fumonisin B₁ (21.2–540 ppm). The feed corn and field corn were also positive for moniliformin (8 and 170 ppm, respectively). In addition, the feed corn also contained low levels of deoxynivalenol (0.9 ppm) and aflatoxins (40.6 ppb).

Among the poultry species, ducklings appear to be most sensitive to moniliformin.¹ Prominent signs and gross changes in experimentally dosed ducklings included dyspnea, lethargy, cyanosis, coma, hemorrhage in the small intestine and kidney, and pericardial edema. Natural occurrences of 28 ppm moniliformin have been previously reported for corn.¹

In contrast, avian deaths associated with high levels of fumonisin B₁ occurring greater than 48 hours after consumption seemed to be due to starvation secondary to feed refusal and reduced intake rather than acute fumonisin toxicity.¹ Fumonisin hepatoxicity and nephrotoxicity have been reported in several species, including rats, horses, pigs, lambs, broilers, turkeys, and ducks.² Similar data do not appear to be available for waterfowl; however, the toxic effects of moniliformin and fumonisins appear to be additive.³ While we suspect that mycotoxins may have caused or contributed to this mortality event, a definitive conclusion has not yet been reached. Whenever mycotoxins are detected, the potential role of other, unidentified mycotoxins, which might have a cumulative or synergistic effect, must also be considered.

Acknowledgments

The authors wish to thank farm manager Don Short, the staff and volunteers at Tri-State for caring for the animals, USGS National Wildlife Health Center pathologists Nancy Thomas, David Green, and Carol Meteyer, and chemistry technician Dan Finley.

References

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2.  Tran ST, Bailly JD, Tardieu S, et al. Sphinganine to sphingosine ratio and predictive biochemical markers of fumonisin B₁ exposure in ducks. Chem Biol Interact. 2003;146:61–72.

3.  Javed T, Bennett GA, Richard MA, et al. Mortality in broiler chicks on feed amended with Fusarium proliferatum culture material, containing known levels of moniliformin, in young broiler chicks. Poult Sci. 1993;74:297–305.