In the fall of 2001, Maryland Department of Natural Resources (MD DNR), US Fish & Wildlife Service (FWS), and Tri-State Bird Rescue and Research (TSBRR) received reports of sick and dead birds. During this time, three separate incidents documenting morbidity and mortality in waterfowl, gulls, and colonial waterbirds occurred. At a private facility in Queen Anne's County, approximately 12 captive waterfowl died over a two-week period; on Poplar Island in Talbot County, an estimated 100 birds of different species died; and in the third event, more than nine great blue herons (GBH; Ardea herodias) were documented dead or dying from three counties. All events showed evidence of a connection with an algal bloom of Microcystis. This report will summarize findings of the GBH event.
On October 18, 2001 the first GBH was found in distress, moribund, was euthanized and sent to the National Wildlife Health Center, Madison, WI, for post mortem examination. Live herons were taken to the TSBRR facility in Newark, DE. Birds presented with clinical signs of emaciation, lethargy, inability to fly, and an unusually hard abdomen. Upon admission to the rehabilitation facility, the birds' blood profiles revealed anemia and varying degrees of hypoproteinemia, and all birds were dehydrated, depressed, in lateral recumbency and had profuse diarrhea. At least two birds were in respiratory distress. Due to poor prognosis, euthanasia was performed and necropsies were conducted on all birds.
Remaining birds were necropsied at the MDDNR Cooperative Oxford Laboratory or at TSBRR. Consistent necropsy findings included emaciation, decreased muscle mass, pale muscle color, fat atrophy, gastrointestinal parasitism, and excessive deposits of waxy, yellow fat in the abdomen, subcutis, and throughout the body cavity. Steatitis was diagnosed in all GBH.
Steatitis is defined as an inflammation of adipose tissue. In mammals, it is associated with a deficiency of vitamin E and /or selenium. Vitamin E and selenium have antioxidant properties and are essential to cell membrane integrity. Interaction between vitamin E / selenium and dietary unsaturated lipids likely play a role in the pathogenesis of steatites, though the exact mechanism is unknown. In birds, this condition is suspected to be caused by a diet high in rancid or oily fish containing polyunsaturated fats. Steatitis has been reported in several other bird species (black crowned night heron Nycticorax nycticorax, osprey Pandion Haliaetus, double crested cormorant Phalocrocorax auritus).
Concurrent with gross necropsy findings, were the unusually large counts of the cyanobacterium (blue-green algae) Microcystis, plus some other cyanobacteria and algae. Microcystis is known to produce the potent cyclic peptide toxins called microcystins. These potential toxin producers were found in water samples collected from the three die-off locales. Microcystins are hepatotoxins produced by at least two Microcystis sp. and several other genera of cyanobacteria. These potent toxins are known to be toxic to fish, mammals (including humans), and birds through skin contact, ingestion, and possibly inhalation. Microcystis sp. are part of a group of microorganisms that are responsible for harmful algal blooms that include: red tides, paralytic and neurotoxic shellfish poisoning, Pfiesteria, etc.
Analysis of water samples from all three events documented the presence of Microcystis at high levels. While analysis of all bird tissues was the goal, due to monetary constraints, only birds from the GBH event were tested for microcystin. Tissue samples were sent to a diagnostic lab with significant experience with toxin identification. Eight samples were analyzed by ELIZA and two by MS/LC, with evidence of toxic levels of microcystin found in the tissue samples.
The investigation is ongoing, and monitoring of great blue herons will continue along with harmful algal bloom monitoring in tributaries of the Chesapeake Bay.