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xi Wildlife biologists once believed that mortality from diseases in wildlife populations was compensatory and, thus, did not affect populations. Instead, they focused on other sources of mortality when conducting population studies. Many avian biologists also held that belief because most disease outbreaks were sporadic and self-limiting, resulting in minor losses. Even then, however, there were localized threats from bird malaria and avian pox virus, for example, to the endangered native bird populations of Hawaii and some large, very localized mortality events among waterbirds from diseases such as avian botulism, avian cholera, and Newcastle disease (Friend et al. 2001). This prevailing perspective changed during the last few decades due to the invasion, emergence, or reemergence of some major diseases of free-ranging wild birds. Avian diseases have increased in frequency of occurrence, prominence , and geographical distribution and resulted in frequently occurring mortality events with major losses of birds of a wide variety of species . Increased attention also resulted from the recognition that 175 new human diseases have emerged in the last two decades, nearly 75% of them caused by zoonotic disease agents that are transmitted among wild or domestic animals and humans (Daszak et al. 2000, Gibbs 2005). Additionally, a troubling number of diseases directly affecting wildlife species and populations emerged (Friend et al. 2001, McLean 2007). Recent avian examples include: the rapid expansion and spread of conjunctivitis caused by Mycoplasma gallisepticum from poultry to House Finches (Carpodacus mexicanus) from the east coast of the United States in 1994 to the Mississippi River (Hartup et al. 2001, Dhondt et al. 2005); a major dieoff of American White Pelicans (Pelacanus erythrorhynchos ) and Brown Pelicans (P. occidentalis) on the Salton Sea in California in 1996 from a unique type C botulism (Rocke et al. 2004); and the dramatic mortality of North American birds from West Nile virus (WNV), especially corvids, American White Pelicans, and Greater Sage-Grouse (Centrocercus urophasianus), following its introduction to North America in 1999 (McLean 2002, Naugle et al. 2004, Rocke et al. 2005, Clark et al. 2006, LaDeau et al. 2007). The establishment and subsequent spread of WNV across the continent within five years of introduction (McLean 2006) was a primary example of an emerging zoonotic disease affecting human, domestic animal, and wildlife populations. The potential threat of direct transmission of WNV and other zoonotic diseases of birds to bird banders and ornithologists led to the development of guidelines and information for wild bird handlers to protect themselves and prevent infection (Ornithological Council 2010). This volume brings together some important information on emerging diseases of wild birds, with topics ranging from how cellular mechanisms of the immune system determine susceptibility to pathogens to the global movement of ticks and bacteria by colonial seabirds. WNV is a central focus, starting with the development of laboratory methods to immunophenotype lymphocytes that FOREWORD xii STUDIES IN AVIAN BIOLOGY NO. 42 Paul determine natural variability in immunocompetence . Two other studies included here on WNV document bird species susceptibility and exposure rates in the southwestern United States. Despite nationally reported mortality from WNV in a number of raptor species in the United States (Nemeth et al. 2006, 2007), including American Kestrels (Falco sparverius), a population study of this species in Colorado found nearly all of the adult birds were immune the year following the 2003 Colorado outbreak. The field study suggests that American Kestrels, at least in Colorado, are not as susceptible to WNV as previously thought and that relatively few birds in the study population died from the infection. Another study of WNV transmission in southern New Mexico revealed differential infection rates among species and habitats. The desert and riparian habitats had higher bird diversity and lower seroprevalence to WNV compared to urban and agriculture habitats. Parasitic disease and vector transmission is another focus of this volume. For example, haemosporidian parasites (Haemoproteus sp.) in endemic Galápagos Doves (Zenaida galapagoensis ), illustrate the negative relationship between host biodiversity and disease prevalence. Host composition significantly affected transmission rates, although other factors affecting disease transmission, particularly vector population dynamics, were mentioned as contributing factors ; these were not directly investigated. The emergence and spread of avian malaria (Plasmodium sp.) is revealed within an endemic population of the New Zealand honeyeater, the Bellbird (Anthornis melanura). A relatively high prevalence of malaria infections was detected without any of the deleterious effects previously observed in the native bird species of Hawaii. Global spread of ticks and Borrelia garinii (a vector and a spirochete), which is a human pathogen...

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