Harmful Algal Blooms and Bird Die-offs in Chesapeake Bay:  A Potential Link?

Barnett A. Rattner, Glenn H. Olsen, Peter C. McGowan, Betty K. Ackerson, and Moira A. McKernan

USGS-Patuxent Wildlife Research Center and Fish and Wildlife Service, Chesapeake Bay Field Office

Autumnal die-offs, involving hundreds of migratory birds, occurred in Chesapeake Bay in 2001, 2004 and 2005.  The most prominent events were at the Poplar Island Complex in proximity to brackish impoundments with algal blooms and elevated cyanobacteria counts (Anabaena spp.).  Although avian botulism was documented as the cause of death of some individuals, recent evidence suggests that cyanobacteria toxin microcystin (MC) may play a role in the initiation of such botulism outbreaks.  During these outbreaks, many dead and dying great blue herons (Ardea herodias) were observed at or near these impoundments at the Poplar Island Complex.  Nearly half (9 of 22) of these individuals collected had detectable quantities of MCs (but not other toxins) in liver tissue, while MCs were not detected in herons collected 50 kilometers southeast at Blackwater NWR.  Affected herons presented clinical signs of emaciation, lethargy, inability to fly, firm distended abdomen, anemia, dehydration and diarrhea.  Rehabilitation efforts were unsuccessful, and moribund birds were euthanized.  Necropsies revealed excessive abdominal deposits of waxy yellow fat (i.e., steatitis, inflammation of the adipose tissue) compared to controls (mean + standard deviation; 371 + 90.6 grams versus 78 + 54.7 grams).  The gastrointestinal tract of affected birds was nearly empty, containing small amounts of greenish vegetation and insects, in contrast to fish found in herons from the reference site.  The most significant hematological changes in affected birds included anemia, depressed plasma cholesterol and potassium, and remarkably low Vitamin E concentration (1.37 + 0.53 µg/ml versus 17.32 + 5.19 of reference herons).  These observations are consistent with historic findings of steatitis in great blue herons from the Chesapeake (Nichols et al. 1986).  We hypothesize several potential causes of steatitis in herons, including (i) a dietary shift by herons to fish species that are high in polyunsaturated fats (e.g., herring)(“Alternate Prey Hypothesis”) (ii) consumption of dead (or possibly dying) rancid fish containing large quantities of oxidized fatty acids (“Rancid Fish Hypothesis”), and/or (iii) exposure to algal toxins by ingestion of water with their prey or indirectly by ingesting prey containing microcystins (“Harmful Algal Bloom Hypothesis”).  In support of this Harmful Algal Bloom Hypothesis, elevated cyanobacteria counts (Anabaena spp.) were detected in impoundments near the die-offs and microcystins were frequently detected in water samples and in liver tissue of dead and dying great blue herons.  Alteration of Vitamin E levels in affected great blue herons is suggestive of depletion of cellular antioxidants (well recognized detoxication response), and possibly one of the independent or inter-related events associated with cellular dysfunction and toxicity evoked by MCs. We hope to more thoroughly investigate the role of MCs and other phycotoxins in recurring waterbird die-offs in Chesapeake Bay through controlled exposure and field investigations.  Such data would provide information on trophic transfer of toxins, and potentially delineate the role of toxins in the development of steatitis in great blue herons.

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