WNV and American White Pelicans | CDC EID

EID Journal Home > Volume 16, Number 3–March 2010

Volume 16, Number 3–March 2010
Research
Surveillance for West Nile Virus in American White Pelicans, Montana, USA, 2006–2007
Gregory Johnson, Nicole Nemeth, Kristina Hale, Nicole Lindsey, Nicholas Panella, and Nicholas Komar
Author affiliations: Montana State University, Bozeman, Montana, USA (G. Johnson, K. Hale); and Centers for Disease Control and Prevention, Fort Collins, Colorado, USA (N. Nemeth, N. Lindsey, N. Panella, N. Komar)

Suggested citation for this article

Abstract
West Nile virus (WNV)–associated deaths of American white pelican (Pelecanus erythrorhynchos) chicks have been recognized at various nesting colonies in the United States since 2002. We evaluated American white pelican nesting colonies in Sheridan County, Montana, USA, for an association between WNV-positive pelican carcasses and human West Nile neuroinvasive disease. Persons in counties hosting affected colonies had a 5× higher risk for disease than those in counties with unaffected colonies. We also investigated WNV infection and blood meal source among mosquitoes and pelican tissue type for greatest WNV detection efficacy in carcasses. WNV-infected Culex tarsalis mosquitoes were detected and blood-engorged Cx. tarsalis contained pelican DNA. Viral loads and detection consistency among pelican tissues were greatest in feather pulp, brain, heart, and skin. Given the risks posed to wildlife and human health, coordinated efforts among wildlife and public health authorities to monitor these pelican colonies for WNV activity are potentially useful.
After West Nile virus (WNV; family Flaviviridae, genus Flavivirus) was detected in the Great Plains of the United States in 2002, programs were initiated to identify the spatial distribution of WNV transmission risk throughout the region. Surveillance activities included compiling case counts for human and equine disease, and testing mosquitoes, avian carcasses, and sentinel chicken serum samples for WNV infection. Corvid (primarily crows and magpies) death surveillance was an effective early warning system for human disease shortly after WNV was detected in this region (1). However, carcasses of numerous other bird species also were positive for WNV (2). Avian deaths caused by WNV infection typically result in widely dispersed carcasses; for the extent of these deaths to be recognized, substantial public cooperation is required in reporting deaths (3). In contrast to this cryptic pattern of deaths, geographically focused deaths among juvenile American white pelicans (Pelecanus erythrorhynchos Gmelin; order Pelecaniformes, family Pelecanidae) have occurred as a result of WNV transmission at numerous pelican-breeding colonies throughout the northern Great Plains (4). This region of the United States has the highest incidence of human West Nile neuroinvasive disease (WNND) recorded (5).

Concurrent with the arrival of WNV to the northern Great Plains region, high death rates of pelican chicks were observed at 4 major colonies in Montana, North Dakota, South Dakota, and Minnesota. WNV was presumed to be the etiologic agent for >9,000 American white pelican deaths in 7 states in 2002–2003 on the basis of testing of a sample of carcasses from various affected colonies (6). At Medicine Lake National Wildlife Refuge (MLNWR) in Montana, the chick death rate from mid-July until fledging, a time when pelican chicks are less vulnerable to severe weather and predation, typically averages <4%. However, this death rate reached as high as 44% among colonies in the region after the arrival of WNV in 2002, and annual losses since then have remained elevated (typically 7–8×) in most years (4). Although a spatiotemporal link between WNV detection and pelican chick deaths seems evident, the cause of most of these deaths remains presumptive. Furthermore, the potential public health consequences of American white pelican deaths need to be evaluated.

Pelican deaths may indicate increased risk for WNV transmission to persons living in nearby communities. We evaluated pelican deaths and human WNND cases for potential associations. In addition, we captured and tested mosquitoes from MLNWR in 2006 and 2007 to determine the risk for vector-borne transmission of WNV and identify the vertebrate source of mosquito blood meals. Finally, we collected a series of tissue types from a subset of pelican carcasses at our field site to identify the most efficient tissue for maximizing the probability of WNV detection and to confirm WNV infection as a contributing factor to elevated prefledgling pelican death rates.

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Suggested Citation for this Article
Johnson G, Nemeth N, Hale K, Lindsey N, Panella N, Komar N. Surveillance for West Nile virus in American white pelicans, Montana, USA, 2006–2007. Emerg Infect Dis [serial on the Internet]. 2010 Mar [date cited].
http://www.cdc.gov/EID/content/16/3/406.htm

DOI: 10.3201/eid1603.090559