Geology topics
F. J. Dein
Publications and source records attributed to F. J. Dein.
Disease emergence in birds: Challenges for the twenty-first century
The paper by Hartup et al. (2001) on House Finch ( Carpodacus mexicanus ) conjunctivitis is an example of the rapid geographic spread that can result from disease emergence in naïve 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. For clarity, we define disease and disease emergence in the context of our use of those terms because they are the focus of our comments. Disease is any departure from health (Guralnik 1982); that is, dysfunction contributing to physiological, physical, reproductive, behavioral, or other impairment that reduces the probability of survival of individuals. If enough individuals are affected, the collective effects can reduce the sustainability of the population. Although disease can result from exposure to a wide variety of physical, chemical, and biological agents and other conditions, we focus this paper on microbes and parasites and to overt mortality caused by them. Thus, disease effects presented only represent the proverbial “tip of the iceberg” relative to the challenges wild avifauna face from disease. Our perspective of disease emergence expands the earlier definitions of emerging diseases by others (Centers for Disease Control and Prevention 1994, Morse 1995) to include all species. Our comments are defined by the context of disease occurrences that have increased within the past three decades, or threaten to increase in the near future relative to populations affected, geographic distribution, or magnitude of effects.
Drowning is not euthanasia
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Special techniques, part E: Flight restraint
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Flight restraint
Many techniques are available for pre ve n ting escape of captive cranes. These include tenotomy, tenectomy, wing clipping, confinement under nets, amputation, brailing, and vane trimming (Ellis and Dein 1991). The advantages and limitations of each technique are presented.
Puerto Rican parrots and potential limitations of the metapopulation approach to species conservation
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Mycotoxin-induced disease in captive whooping cranes (Grus americana) and sandhill cranes (Grus canadensis)
In 1987, an epizootic in cranes at the Patuxent Wildlife Research Center, Laurel, Maryland, USA, caused illness in 80% of 300 captive whooping cranes (Grus americana) and sandhill cranes (Grus canadensis) and death of 15 of these cranes. Gross pathology findings were inconclusive and consisted of dehydration, atrophy of fat, renal insufficiency, and small spleens. Extensive testing resulted in isolation of Fusarium sp. mold from constituents of the grain-based diet. Low levels of two mycotoxins, T2 (1-2 ppm) and deoxynivalenol (0.4 ppm), were isolated from the pelleted feed.
Prevention of eastern equine encephalitis virus in captive cranes
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Surgical removal of a tracheal foreign body from a whooping crane (Grus americana)
The left wing of a whooping crane (Grus americana) was amputated for treatment of severe nonunion and malunion fractures of the radius and ulna. During the postoperative convalescent period, the bird aspirated a corn kernel and subsequently suffered episodic bouts of dyspnea. The bird was anesthetized with tiletamine-zolazepam. Attempts to deliver the kernel through the glottis with endoscopic instruments were unsuccessful. The corn kernel was retrieved via a tracheotomy incision. Endoscopy of the trachea 2 mo postoperatively showed complete healing of the tracheal incision. Mucosal integrity had been reestablished, and tracheal lumen diameter was not compromised. The bird continues in good health 2.5 yr after surgery, shows no sign of respiratory disease, and currently is in a captive breeding program.
Tuberculosis in wild birds: implications for captive birds
The geographic distribution of avian tuberculosis is widespread but the lack of visible epizootics makes assessment of its impact on wild birds difficult. Generally a low prevalence, widely-scattered, individual animal disease, avian tuberculosis is caused by the same agent in wild and domestic birds. Thus there exists the potential for disease transfer between these two groups in situations that result in direct contact such as wild animals newly captured or transferred from rehabilitation centers, and wild and captive animals intermingling in exhibit areas. During the past 7 yr, tuberculosis caused by Mycobacterium avium, was diagnosed in 64 birds submitted to the National Wildlife Health Research Center from 16 states; avian tuberculosis was the primary diagnosis in 52 of the 64 birds, while the remaining 12 isolates were incidental findings. Twenty-eight of these birds were picked up during epizootics caused by other disease agents including avian cholera, botulism type C, and lead, organophosphorus compound, and cyanide poisoning. Twelve birds were found incidental to birds collected during disease monitoring programs and research projects, and 10 birds were collected by hunters or found sick and euthanatized. Tuberculosis lesions occurred (in order of decreasing frequency) in the liver, intestine, spleen, lung, and air sacs. Several unusual morphological presentations were observed in the gizzard, shoulder joint, jugular vein, face, nares and bill, ureter and bone marrow. Infected birds were collected during all 12 mo of the yr from a variety of species in the Anseriformes, Podicipediformes, Gruiformes, and Falconiformes. Nine of the 46 known age birds were immature indicating that lesions can develop during the first year.
Antibody response of sandhill and whooping cranes to an eastern equine encephalitis virus vaccine
As a possible strategy to protect whooping cranes (Grus americana) from fatal eastern equine encephalitis (EEE) viral infection, studies were conducted to determine the immune response of this species and sandhill cranes (Grus canadensis) to a formalin-inactivated EEE viral vaccine. Viral-specific neutralizing antibody was elicited in both species after intramuscular (IM) vaccination. Subcutaneous and intravenous routes of vaccination failed to elicit detectable antibody in sandhill cranes. Among the IM vaccinated cranes, the immune response was characterized by nondetectable or low antibody titers that waned rapidly following primary exposure to the vaccine. However, one or more booster doses consistently elicited detectable antibody and/or increased antibody titers in the whooping cranes. In contrast, cranes with pre-existing EEE viral antibody, apparently induced by natural infection, exhibited a rapid increase and sustained high-antibody titers. Even though EEE virus vaccine induced neutralizing antibody and produced no adverse side effects, further studies will be required to determine the protective efficacy of the antibody.
An outbreak of eastern equine encephalitis virus in captive whooping cranes
No abstract available.
Mortality of captive whooping cranes caused by eastern equine encephalitis virus
Of 39 captive whooping cranes (Grus americana), 7 died during a 7-week period (Sept 17 through Nov 4, 1984) at the Patuxent Wildlife Research Center, Laurel, Md. Before their deaths, 4 cranes did not develop clinical signs, whereas the other 3 cranes were lethargic and ataxic, with high aspartate transaminase, gamma-glutamyl transferase, and lactic acid dehydrogenase activities, and high uric acid concentrations. Necropsies indicated that the birds had ascites, intestinal mucosal discoloration, fat depletion, hepatomegaly, splenomegaly, and visceral gout. Microscopically, extensive necrosis and inflammation were seen in many visceral organs; the CNS was not affected. Eastern equine encephalitis (EEE) virus was isolated from specimens of the livers, kidneys, lungs, brains, and intestines of 4 of the 7 birds that died, and EEE virus-neutralizing antibody was detected in 14 (44%) of the 32 surviving birds. Other infectious or toxic agents were not found. Morbidity or mortality was not detected in 240 sandhill cranes (Grus canadensis) interspersed among the whooping cranes; however, 13 of the 32 sandhill cranes evaluated had EEE virus-neutralizing antibody. Of the 41 wild birds evaluated in the area, 3 (4%) had EEE virus-neutralizing antibody. Immature Culiseta melanura (the most probable mosquito vector) were found in scattered foci 5 km from the research center.
Use of an inactivated eastern equine encephalitis virus vaccine in cranes
An unprecedented outbreak of fatal eastern equine encephalitis (EEE) virus occurred during the late summer and fall of 1984 in endangered whooping cranes (Grus americana) at the Patuxent Wildlife Research Center, Laurel, Maryland. As part of efforts to prevent future epizootics of EEE. studies were conducted to evaluate the antibody response of cranes following vaccination with a formalin-inactivated EEE virus vaccine. Viral specific neutralizing antibody was elicited in sandhill cranes (Grus canadensis) and whooping cranes following 1M inoculation with the vaccine. Among the 1M-inoculated cranes, peak antibody titers of 1:80 on days 30 to 60 had waned to undetectable levels by days 90 to 120. Although the initial titers were not increased by the first booster dose, the duration of the antibody was extended considerably. Whooping cranes, receiving vaccine 6 months after their first vaccination, developed titers of 1:80 to 1:320 by day 30. At 45 days after the final vaccination, these titers had dropped to 1:10 to 1:160. Cranes with preexisting EEE virus antibody, apparently reflecting natural infection, exhibited an anamnestic response indicated by a rapid increase and sustained high antibody titer. Even though EEE virus vaccine induced neutralizing antibody and produced no adverse side effects, further studies will be required to assess the significance of this response as a strategy for protecting whooping cranes against natural EEE virus infection. The loss of captive whooping cranes to the EEE virus presented a previously unrecognized risk and obstacle to recovery of this species. Not only was, there a setback in the captive breeding and reintroduction program for the whooping crane, but, because of the susceptibility of the species to the EEE virus. establishment of additional crane populations may be more complicated than initially envisioned. However, through continued surveillance, serological monitoring, and vaccination activities, we are confident that the impact of EEE virus on whooping crane recovery can be overcome to the ultimate benefit of this endangered species.
The Andean condor as a research surrogate for the California condor
Captive propagation of Andean Condors ( Vultur gryphus ) was initiated at the Patuxent Wildlife Research Center in 1966 in anticipation of the need to apply resulting techniques to the captive breeding of the endangered California Condor ( Gymnogyps californianus ). This report summarizes the progress made on this Andean Condor breeding and research project, with emphasis on recent fostering/cross-fostering studies. These studies include: (a) fostering eggs/chicks between Andean Condors; (b) fostering of two chicks each to Andean Condor pairs; (c) cross-fostering of a Turkey Vulture ( Cathartes aura ) to Andean Condors; and (d) cross-fostering an Andean Condor chick to wild California Condors. Implications of these studies for the recovery of the California Condor will be discussed.
An epizootic of eastern equine encephalitis virus in whooping cranes
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