Geology topics
F. J. Dein
Publications and source records attributed to F. J. Dein.
Limited infection upon human exposure to a recombinant raccoon pox vaccine vector
A laboratory accident resulted in human exposure to a recombinant raccoon poxvirus (RCN) developed as a vaccine vector for antigens of Yersinia pestis for protection of wild rodents (and other animals) against plague. Within 9 days, the patient developed a small blister that healed within 4 weeks. Raccoon poxvirus was cultured from the lesion, and the patient developed antibody to plague antigen (F1) and RCN. This is the first documented case of human exposure to RCN.
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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Sodium toxicity and pathology associated with exposure of waterfowl to hypersaline playa lakes of southeast New Mexico
Cause of mortality was studied in waterfowl in hypersaline playa lakes of southeast New Mexico during spring and fall migration. Mortality was not common in wild ducks resting on the playas during good weather. However, when birds remained on the lakes for prolonged periods of time, such as during experimental trials and stormy weather, a heavy layer of salt precipitated on their feathers. Sodium toxicity was the cause of death for all experimental mallards housed on playa water and for 50% of the wild waterfowl found moribund or dead during the spring of 1995. Gross lesions included heavy salt precipitation on the feathers, ocular lens opacities, deeply congested brains, and dilated, thin-walled, fluid-filled cloacae. Microscopic lesions in the more severely affected birds included liquefaction of ocular lens cortex with lens fiber swelling and multifocal to diffuse ulcerative conjunctivitis with severe granulocytic inflammation, edema, and granulocytic vasculitis resulting in thrombosis. Inflammation similar to that seen in the conjunctiva occasionally involved the mucosa of the mouth, pharynx, nasal turbinates, cloaca, and bursa. Transcorneal movement of water in response to the hypersaline conditions on the playa lakes or direct contact with salt crystals could induce anterior segment dehydration of the aqueous humor and increased osmotic pressure on the lens, leading to cataract formation.
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.
Avian leucocyte counting using the hemocytometer
Automated methods for counting leucocytes in avian blood are not available because of the presence of nucleated erythrocytes and thrombocytes. Therefore, total white blood cell counts are performed by hand using a hemocytometer. The Natt and Herrick and the Unopette methods are the most common stain and diluent preparations for this procedure. Replicate hemocytometer counts using these two methods were performed on blood from four birds of different species. Cells present in each square of the hemocytometer were counted. Counting cells in the corner, side, or center hemocytometer squares produced statistically equivalent results; counting four squares per chamber provided a result similar to that obtained by counting nine squares; and the Unopette method was more precise for hemocytometer counting than was the Natt and Herrick method. The Unopette method is easier to learn and perform but is an indirect process, utilizing the differential count from a stained smear. The Natt and Herrick method is a direct total count, but cell identification is more difficult.
Vitamin E in cranes: Reference ranges and nutrient interactions
Fat soluble vitamins E and A (quantified as α-tocopherol and all-trans retinol, respectively) were measured in plasma samples from 274 captive cranes from four institutions and five free-ranging birds. Ages ranged from 4 mo to 80 yr, and all 15 crane species were represented. Captive cranes had a mean ± standard error (SE) of 6.57 ± 0.82 μ g/ml α -tocopherol; migrating greater sandhill cranes ( Grus canadenis tabida ) had a plasma concentration of 3.71 ± 0.22 μ g/ml. Sex and age differences were not significant, but crane species that evolved in temperate habitats had higher circulating levels of α -tocopherol than tropical or subtropical species. Mean ± SE retinol values were 0.69 ± 0.05 μ g/ml in captive cranes, and 0.66 ± 0.08 μ g/ml in free-ranging cranes; values did not differ significantly by sex, age, or species. Dietary vitamin E concentrations were significantly correlated with plasma α -tocopherol levels in a logarithmic relationship. Dietary selenium at 0.5 mg/kg was associated with decreased circulating a-tocopherol concentrations.
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.
Flight restraint techniques for captive cranes
Traditional techniques for preventing escape of captive cranes (i.e., tenotomy, tenectomy, wing clipping, confinement under nets, and amputation) are discussed briefly. Two additional techniques (i.e., brailing and vane trimming) are described in detail. The advantages and limitations of each technique are presented.
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.