38 research outputs found

    DISEASE EMERGENCE IN BIRDS: CHALLENGES FOR THE TWENTY-FIRST CENTURY

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    Finch (Carpodacus mexicanus) conjunctivitis is an example of the rapid geographic spread that can result from disease emergence in naive populations. That event was neither novel nor transient relative to its occurrence or effects. Disease emergence and reemergence are hallmarks of the latter part of the twentieth century (Center for Disease Control 1994, Levins et al. 1994, DaSilva and Laccarino 1999, Gratz 1999). Current examples involving domestic animals include the problems in Europe with bovine spongiform encephalopathy (BSE, or ‘‘mad cow disease’’) (Brown 2001) and foot-and-mouth disease (FMD) (Kitching 1999). Human health has been affected by diseases caused by an array of viruses (Morse 1993, Nichol et al. 1993, Murphy and Nathanson 1994), bacteria (Dennis 1998, DaSilva and Laccarino 1999), rickettsia (Walker and Dumier 1996, Azad et al. 1997), protozoans (Tuerrant 1997, Saini et al. 2000), and metazoan parasites (Hildreth et al. 1991, Gubler 1998), as well as other causes. Acquired immune deficiency syndrome (AIDS) has received the most notoriety of those diseases (Hahn et al. 2000, Schwartlander et al. 2000). A similar pattern exists on a global scale for free-ranging wildlife populations (Table 1) (Friend 1994, 1995; Epstein et al. 1998, Daszak et al. 2000). However, in comparison to disease emergence affecting humans and domestic animals, response to emerging diseases of wildlife is generally superficial. We present concepts and data to support our contention that failure to adequately address disease emergence in free-ranging wildlife is resulting in a diminished capability to achieve and sustain desired geographic distributions and population abundance for species of wild birds, including some threatened and endangered avifauna

    DISEASE EMERGENCE IN BIRDS: CHALLENGES FOR THE TWENTY-FIRST CENTURY

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    Disease Emergence and Resurgence: The Wildlife-Human Connection

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    Humans have been affected by and have contributed to the eruption and spread of disease since antiquity. This connectivity is such that disease in the Americas was one of the five Seeds of Change addressed by the National Museum of Natural History’s commemoration of the Columbus Quincentenary. As for the other Seeds of Change, diseases “…sent ripples around the globe, affecting the people as well as the flora and fauna of both the New World and the Old.” During recent decades, these ripples have become waves that are likely to intensify, swelled by human population growth, civil strife, and other factors. Similar to the Columbus voyages of discovery, disease emergence involves the processes of encounter and exchange resulting in both deliberate and accidental introductions. Biowarfare was the primary purpose for past deliberate disease introductions in the Americas (e.g., smallpox during the French and Indian Wars). Bioterrorism is the primary focus for current introductions (e.g., post-9/11 anthrax letters). Ecosystem alteration is a human hallmark with direct and indirect consequences for disease, especially for zoonoses. Large-scale landscape alteration will continue to occur due to human population growth and technological advancement. These transformations not only enhance the processes of encounter and exchange between organisms as a factor for disease emergence, but they also can greatly accelerate evolutionary changes, especially in disease organisms. Clearly, disease continues as an important “seed of change” sowed by human actions that result in the emergence of new global challenges for society. The context for this book focuses on providing an understanding that disease emergence and spread often are outcomes of human actions, rather than the result of events for which society has no control

    Fungal Diseases (Field Manual of Wildlife Diseases)

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    Fungi are important causes of disease in wild birds and other species. Three basic types of disease are caused by these agents: mycosis, or the direct invasion of tissues by fungal cells, such as aspergillosis; allergic disease involving the development of a hypersensitivity of the host to fungal antigens; and mycotoxicosis, which results from ingestion of toxic fungal metabolites. Mycosis and allergic disease may occur together, especially when the lung is infected. This section will address only mycosis. Mycotoxicosis is addressed in Section 6, Biotoxins. Allergic disease is not well studied in wild birds and it is beyond the scope of this Manual. Most disease-causing fungi are commonly found within the normal environment of hosts that may become diseased. Host resistance is the main determinant of whether or not disease will occur. Opportunistic infections often result when birds and other species are immunosuppressed, when their mechanisms for inflammatory response are inhibited, or when they experience physical, nutritional, or other stress for prolonged periods of time. Newborn do not have fully functioning immune systems and are, therefore, especially vulnerable to mycosis as are very old animals that are likely to have impaired immune systems. Inhalation is the primary route for exposure to most fungi-causing mycosis. Aspergillosis is the primary mycosis affecting wild birds. Candidiasis is a less common mycosis of wild birds and other species, but it differs greatly from aspergillosis by being transmitted by ingestion. These two diseases are the primary mycoses of wild birds and are the main subjects of this section

    13.2.6. Lead Poisoning: The Invisible Disease

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    Lead poisoning is an intoxication resulting from absorption of hazardous levels of lead into body tissues. Lead pellets from shot shells, when ingested, are the most common source of lead poisoning in migratory birds. Other far less common sources include lead fishing sinkers, mine wastes, paint pigments, bullets, and other lead objects that are swallowed

    Bacterial Diseases (Field Manual of Wildlife Diseases)

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    Diseases caused by bacteria are a more common cause of mortality in wild birds than are those caused by viruses. In addition to infection, some bacteria cause disease as a result of potent toxins that they produce. Bacteria of the genus Clostridium are responsible for more wild bird deaths than are other disease agents. Clostridium botulinum, which causes avian botulism, is primarily a form of food poisoning and it is included within the section on biotoxins (see Chapter 38). Other Clostridium sp. that colonize intestinal tissues produce toxins that cause severe hemorrhaging of the intestine, thus leading to tissue death or necrosis and intoxication of the bird due to the exotoxins produced by the bacterial cell. The descriptive pathology is referred to as a necrotizing gastroenteritis or necrotic enteritis and the disease as clostridial enterotoxemia. The classic example in gallinaceous birds such as quail, turkey, pheasant, grouse, and partridge, is ulcerative enteritis or quail disease, which is caused by Clostridium colinium; quail are the species most susceptible to that disease. Necrotic enteritis of wild waterbirds, especially geese, has been reported with increasing frequency during recent years. Clostridium perfringens has been associated with these deaths

    13.2.5. Avian Cholera: A Major New Cause of Waterfowl Mortality

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    Avian cholera is a highly infectious disease caused by the bacterium, Pasteurella multocida. Acute infections are common and can result in death 6 to 12 hours after exposure. Under these circumstances “explosive” die-offs involving more than 1,000 birds per day have occurred in wild waterfowl. More chronic infections with longer incubation times and less dramatic losses also occur. Transmission can occur by bird-to-bird contact, ingestion of contaminated food or water, and perhaps in aerosol form

    Chemical Toxins (Field Manual of Wildlife Diseases)

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    Many kinds of potentially harmful chemicals are found in environments used by wildlife. Some chemicals, such as pesticides and polychlorinated biphenyls (PCBs), are synthetic compounds that may become environmental contaminants through their use and application. Other materials, such as selenium and salt, are natural components of some environments, but contaminants of others. Natural and synthetic materials may cause direct poisoning and death, but they also may have adverse effects on wildlife that impair certain biological systems, such as the reproductive and immune systems. This section provides information about some of the environmental contaminants and natural chemicals that commonly cause avian mortality; microbial and other biotoxins are addressed in the preceding section. Direct poisoning and mortality of wildlife caused by exposure to chemical toxins are the focus of this section. However, the indirect effects of chemicals may have significantly greater impacts on wildlife populations than the direct effects. Behavioral changes that affect survival, reproductive success and the survival of young, and that impair the functioning of the immune system are examples of indirect chemical toxicity that are known to occur but that are beyond the scope of this publication. For additional information readers are directed to more comprehensive treatments of environmental toxicology and to publications that focus on specific chemicals and their effects on wildlife. The diagnosis of chemical poisoning as the cause of wildlife mortality is a challenging task because of the vast array of chemicals that wildlife may be exposed to (Table 1), the variable biological responses following concurrent exposure to multiple chemicals, the absence of tissue residues for some chemical toxins, and the lack of specific pathological changes associated with most chemical toxins in tissues. The diagnostic process can be greatly facilitated by a thorough field observation record, comprehensive background information about the circumstances of a mortality event, and by properly collecting, handling, and preserving samples submitted to the diagnostic laboratory (see Section 1). Sources of assistance for the investigation of wildlife mortality, when toxins are suspected, are listed in Appendix B
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