The decline of the bald eagle parallels that of the Indian vulture, says S.Ananthanarayanan.

The Indian vulture, descendant of the legendary Jatayu, of the Ramayana, faces extinction because of a popular veterinary medicine, which is toxic to vultures that feed on animal carcasses. The bald eagle, found in North America, and some other bird, amphibian, reptile and fish species, are now in danger because of a similar reason, a substance used as a weed killer in large water bodies.

Steffen Breinlinger, Tabitha J. Phillips, Brigette N. Haram, Jan Mareš, José A. Martínez Yerena, Pavel Hrouzek, Roman Sobotka, W. Matthew Henderson, Peter Schmieder, Susan M. Williams, James D. Lauderdale, H. Dayton Wilde, Wesley Gerrin, Andreja Kust, John W. Washington, Christoph Wagner, Benedikt Geier, Manuel Liebeke, Heike Enke, Timo H. J. Niedermeyer, Susan B. Wilde, from Martin-Luther-University Halle-Wittenberg, Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Berlin, and Planck Institute for Marine Microbiology, Bremen, Germany, the Czech Academy of Sciences and the University of South Bohemia, Czech Republic , University of Georgia, USA and the U.S. Environmental Protection Agency, describe in the journal, Sciencethe course of detecting the agent behind the loss of eagles in North America.

Over the winter of 1994 to 1995, the paper says, there was unprecedented mortality of bald eagles at DeGray Lake in Arkansas, USA. The cause of eagle deaths was found to be a neurodegenerative disease, avian vacuolar myelinopathy (AVM), which destroyed brain tissue and led to birds losing control over their bodies. The birds would “overfly perches and collide with rock walls”, says a publication. In the three years that followed, the same disease was confirmed in five other states and in many other avian species. The outbreaks were during the fall and winter and in or near man-made water bodies which had abundant aquatic vegetation. Good numbers of fish and water birds in the winter months attract bald eagles. The water birds were affected by AVM and were easy targets. But they passed the disease on to the predators.

It was found that wild coots and mallards developed AVM within five weeks of being released into a lake which had the disease. Chemical analyses of bird carcasses, however, revealed no traces of chemicals which could be responsible. The material from affected lakes and ponds did not induce disease and the disease did not transfer from one bird to another. The source of the disease was elusive!

Then, it was found that all the disease-affected water bodies contained rapidly spreading, or invasive, underwater vegetation, mainly Hydrilla verticillata, or waterthyme, with the leaves heavily colonized by a previously unidentified form of blue-green algae. And it was shown that AVM was induced in water birds when they fed on Hydrilla verticillata which had the algae. The algae have been named Aetokthonos hydrillicola – Greek for ‘eagle-killer that resides on hydrilla’. And then, as AVM was also found to affect amphibians, reptiles and fish, the letter, ‘A’ has been dropped from the acronym, leaving it as ‘VM’.

As blue-green algae, also known as cyanobacteria, are known to participate in production of toxins and other specialised chemicals, it was possible that the A. hydricillicola on the leaves was responsible for the outbreak of VM. The paper states that H. verticillate, colonized by A. hydricillicola, was found to be widespread in major water bodies throughout southeastern United States. The team hence collected samples of the plant and its coloniser, to isolate and culture the cyanobacterium, and then to track down the neurotoxin.

The process took two years, the paper says, but A. hydricillicola was successfully cultured. And the culture was also confirmed as A. hydricillicola, by testing for a specific genetic component. However, administering the substance to experimental chickens did not result in VM. The idea that A. hydricillicola produced the toxin was hence not borne out. Could it be that the cyanobacterium produces the suspected toxin only when it grows on H. ventricillata, and not when cultured in the lab?

To test this possibility, the team collected more A. hydrillicola, not from cultures, but as growing on H. verticillate from water bodies that were known to host VM. The colonies of cyanobacteria were then analysed using a complex laboratory technique which could identify individual compounds in a mixture of many. The procedure detected a molecule that contained, like many organic substances, atoms of carbon, hydrogen and nitrogen, and in addition, a good number of atoms of bromine. Significantly, this molecule was not there in the cyanobacteria grown in the lab. It was apparent that the molecule was a new one that arose when the cyanobacterium colonized the water plants, and could be the reason for VM. The paper also notes that compounds containing bromine or chlorine are known to produce VM-like brain lesions.

Control trials were now conducted by adding bromine sources to the laboratory cultures. The result, sure enough, was that the cultures now led to VM – which showed that it was bromine that made the difference. Further trials could show how varying the level of bromine affected the production of the toxin. And more important, that the environmental stress of lower temperatures, as found in the fall and in winter, led to the greatest production.

Sources of bromine

The presence of bromine in the water bodies may be partly natural, and partly the chemicals used by power plants or inflows like fungicides, gasoline additives, that flow in. Chemicals used to control the rapid increase of underwater plants, including H. ventricillata, contain bromine, the paper says. The paper mentions a biological means of controlling weeds, a species of fish that could deal with excess plants. This is a solution that has been used to eliminate H. ventricillata in places where there were eagle deaths, the paper says. There is reluctance on the part of fisheries managers, the paper says, but the concerns need to be assessed and benefits of using chemicals need to be reviewed.

That there is a study and steps have been taken to regulate the use of bromine-containing substances suggests that inadvertent damage to an important part of biodiversity would now be prevented. In the case of the Indian vulture, rapid decline in numbers, due to kidney disease, was noticed in the 1990s. In 2003, the Peregrine Fund, which had helped save the peregrine falcon in the US, identified the cause as the drug, diclofenac, a drug that is used to relieve joint pain and swelling. A veterinary preparation was also widely used with cattle. When vultures, which forage in flocks, fed on carcasses of the cattle, they ingested diclofenac and started dying in numbers.

Despite lobbying by wild life conservation groups, the Indian authorities were slow to ban the veterinary drug. Even after the ban, dairy farmers use, not an alternative that is available, but the human version of the drug with declofenac, which does not help the Indian vulture. The bird is now scarcely seen and is said to be there in captive breeding.

The vulture in Eurpope

In 2016, the journal Nature cited a current paper in the Journal of Applied Ecology, which said diclofenac, which has been approved in Spain, endangers thousands of that country’s Eurasian griffon vultures.
“In Europe, diclofenac has been approved for veterinary use since 1993. In 2014, the European Medicines Agency acknowledged that vultures are at risk of consuming residues of the drug in dead livestock, but did not recommend banning it. In 2015, the European Commission decided to follow the EMA’s recommendation, leaving it up to EU member states to prevent diclofenac-laced carcasses from entering the food chain,” the news item in Nature said.

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