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R. McLean

Publications and source records attributed to R. McLean.

4 recordsLinked to original sources

The impact of disease in the American white pelican in North America

Records of reported die-offs of the American White Pelican (Pelicanus erythrorhynchos) held by the U.S. Geological Survey National Wildlife Health Center from 1978 through 2003 indicate that type C botulism (caused by Clostridium botulinum) was the major cause of mortality. In 1996, over 15,000 birds, including 8,500 American White Pelicans, were estimated to have died from type C botulism at the Salton Sea in California. This was the largest documented die-off of any pelican species and was estimated to represent 15-20% of the western metapopulation. This event was also notable in that it was the first time that fish, specifically Tilapia (Oreochromis mossambicus), were implicated as the source of type C botulinum toxin for birds. Type C botulism has recurred in both North American species of pelicans at the Salton Sea every year since, although the magnitude of mortality is much lower. West Nile virus caused mortality in both adult and immature American White Pelicans, but may have a more significant impact on nestlings. Emaciation and mortality is common in pelican nesting colonies. Further clarification of the cause of nestling mortality and the ability to differentiate background mortality from mortality due to infectious disease agents such as West Nile virus and Newcastle disease virus would be important in determining the impact of disease in pelicans. Although definitive conclusions cannot be drawn, the number of die-offs and the estimated losses of American White Pelicans appears to have increased along with declines in number in western U.S.

Waterbirds↗

West Nile Virus and wildlife

West Nile virus (WNV) has spread rapidly across North America, resulting in human deaths and in the deaths of untold numbers of birds, mammals, and reptiles. The virus has reached Central America and the Caribbean and may spread to Hawaii and South America. Although tens of thousands of birds have died, and studies of some bird species show local declines, few regionwide declines can be attributed to WNV. Predicting future impacts of WNV on wildlife, and pinpointing what drives epidemics, will require substantial additional research into host susceptibility, reservoir competency, and linkages between climate, mosquitoes, and disease. Such work will entail a collaborative effort between scientists in governmental research groups, in surveillance and control programs, and in nongovernmental organizations. West Nile virus was not the first, and it will not be the last, exotic disease to be introduced to the New World. Its spread in North America highlights the need to strengthen animal monitoring programs and to integrate them with research on disease ecology.

BioScience↗

Detection of West Nile virus infection in birds in the United States by blocking ELISA and immunohistochemistry

A blocking ELISA targeting an immunodominant West Nile epitope on the West Nile Virus NS1 protein was assessed for the detection of West Nile–specific antibodies in blood samples collected from 584 sentinel chickens and 238 wild birds collected in New Jersey from May–December 2000. Ten mallard ducks ( Anas platyrhynchos ) experimentally infected with West Nile virus and six uninfected controls were also tested. The ELISA proved specific in detecting WNV antibodies in 9/10 chickens and 4/4 wild birds previously confirmed as positive by Plaque Reduction Neutralization test (PRNT) at the Center for Disease Control, Division of Vector Borne Diseases, Fort Collins, CO, USA (CDC). Nine out of the ten experimentally infected mallard ducks also tested positive for WN antibodies in the blocking ELISA, while 6/6 uninfected controls did not. Additionally, 1705 wild birds, collected in New Jersey from December 2000–November 2001 and Long Island, New York between November 1999 and August 2001 were also tested for WN antibodies by the blocking ELISA. These tests identified 30 positive specimens, 12 of which had formalin-fixed tissues available to allow detection of WN specific viral antigen in various tissues by WNV-specific immunohistochemistry. Our results indicate that rapid and specific detection of antibodies to WN virus in sera from a range of avian species by blocking ELISA is an effective strategy for WN Virus surveillance in avian hosts. In combination with detection of WN-specific antigens in tissues by immunohistochemistry (IHC) the blocking ELISA will also be useful for confirming WN infection in diseased birds.

Colorado, New Jersey, New York↗

Crow deaths as a sentinel surveillance system for West Nile virus in the northeastern United States, 1999

In addition to human encephalitis and meningitis cases, the West Nile (WN) virus outbreak in the summer and fall of 1999 in New York State resulted in bird deaths in New York, New Jersey, and Connecticut. From August to December 1999, 295 dead birds were laboratory-confirmed with WN virus infection; 262 (89%) were American Crows ( Corvus brachyrhynchos ). The New York State Department of Health received reports of 17,339 dead birds, including 5,697 (33%) crows; in Connecticut 1,040 dead crows were reported. Bird deaths were critical in identifying WN virus as the cause of the human outbreak and defining its geographic and temporal limits. If established before a WN virus outbreak, a surveillance system based on bird deaths may provide a sensitive method of detecting WN virus.

Connecticut, New Jersey, New York↗