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Carol U. Meteyer

Publications and source records attributed to Carol U. Meteyer.

At least 37 records · Page 2Linked to original sources
USGS2012

Histopathology confirms white-nose syndrome in bats in Europe

White-nose syndrome, associated with the fungal skin infection geomycosis, caused regional population collapse in bats in North America. Our results, based on histopathology, show the presence of white-nose syndrome in Europe. Dermatohistopathology on two bats (Myotis myotis) found dead in March 2010 with geomycosis in the Czech Republic had characteristics resembling Geomyces destructans infection in bats confirmed with white-nose syndrome in US hibernacula. In addition, a live M. myotis, biopsied for histopathology during hibernation in April 2011, had typical fungal infection with cupping erosion and invasion of muzzle skin diagnostic for white-nose syndrome and conidiospores identical to G. destructans that were genetically confirmed as G. destructans.

Journal of Wildlife Diseases↗
USGS2012

Comparative risk assessment of the first-generation anticoagulant rodenticide diphacinone to raptors

New regulatory restrictions have been placed on the use of some second-generation anticoagulant rodenticides in the United States, and in some situations this action may be offset by expanded use of first-generation compounds. We have recently conducted several studies with captive adult American kestrels and eastern screech-owls examining the toxicity of diphacinone (DPN) using both acute oral and short-term dietary exposure regimens. Diphacinone evoked overt signs of intoxication and lethality in these raptors at exposure doses that were 20 to 30 times lower than reported for traditionally used wildlife test species (mallard and northern bobwhite). Sublethal exposure of kestrels and owls resulted in prolonged clotting time, reduced hematocrit, and/or gross and histological evidence of hemorrhage at daily doses as low as 0.16 mg DPN/kg body weight. Findings also demonstrated that DPN was far more potent in short-term 7-day dietary studies than in single-day acute oral exposure studies. Incorporating these kestrel and owl data into deterministic and probabilistic risk assessments indicated that the risks associated with DPN exposure for raptors are far greater than predicted in analyses using data from mallards and bobwhite. These findings can assist natural resource managers in weighing the costs and benefits of anticoagulant rodenticide use in pest control and eradication programs.

Conference Paper↗
USGS2011

Acute toxicity, histopathology, and coagulopathy in American kestrels (Falco sparverius) following administration of the rodenticie diphacinone

The acute oral toxicity of the anticoagulant rodenticide diphacinone was found to be over 20 times greater in American kestrels (Falco sparverius; median lethal dose 96.8 mg/kg body weight) compared with Northern bobwhite (Colinus virginianus) and mallards (Anas platyrhynchos). Modest evidence of internal bleeding was observed at necropsy, although histological examination of heart, liver, kidney, lung, intestine, and skeletal muscle revealed hemorrhage over a wide range of doses (35.1-675 mg/kg). Residue analysis suggests that the half-life of diphacinone in the liver of kestrels that survived was relatively short, with the majority of the dose cleared within 7 d of exposure. Several precise and sensitive clotting assays (prothrombin time, Russell's viper venom time, thrombin clotting time) were adapted for use in this species, and oral administration of diphacinone at 50 mg/kg increased prothrombin time and Russell?s viper venom time at 48 and 96 h postdose compared with controls. Prolongation of in vitro clotting time reflects impaired coagulation complex activity, and generally corresponded with the onset of overt signs of toxicity and lethality. In view of the toxicity and risk evaluation data derived from American kestrels, the involvement of diphacinone in some raptor mortality events, and the paucity of threshold effects data following short-term dietary exposure for birds of prey, additional feeding trials with captive raptors are warranted to characterize more fully the risk of secondary poisoning.

Environmental Toxicology and Chemistry↗
USGS2011

Copper pellets simulating oral exposure to copper ammunition: Absence of toxicity in American kestrels ( Falco sparverius )

To evaluate the potential toxicity of copper (Cu) in raptors that may consume Cu bullets, shotgun pellets containing Cu, or Cu fragments as they feed on wildlife carcasses, we studied the effects of metallic Cu exposure in a surrogate, the American kestrel ( Falco sparverius ). Sixteen kestrels were orally administered 5 mg Cu/g body mass in the form of Cu pellets (1.18–2.00 mm in diameter) nine times during 38 days and 10 controls were sham gavaged on the same schedule. With one exception, all birds retained the pellets for at least 1 h, but most (69%) regurgitated pellets during a 12-h monitoring period. Hepatic Cu concentrations were greater in kestrels administered Cu than in controls, but there was no difference in Cu concentrations in the blood between treated and control birds. Concentration of the metal-binding protein metallothionein was greater in male birds that received Cu than in controls, whereas concentrations in female birds that received Cu were similar to control female birds. Hepatic Cu and metallothionein concentrations in kestrels were significantly correlated. Histopathologic alterations were noted in the pancreas of four treated kestrels and two controls, but these changes were not associated with hepatic or renal Cu concentrations, and no lesions were seen in other tissues. No clinical signs were observed, and there was no treatment effect on body mass; concentrations of Cu, hemoglobin, or methemoglobin in the blood; or Cu concentrations in kidney, plasma biochemistries, or hematocrit. Based on the parameters we measured, ingested Cu pellets pose little threat to American kestrels (and presumably phylogenetically related species), although the retention time of pellets in the stomach was of relatively short duration. Birds expected to regurgitate Cu fragments with a frequency similar to kestrels are not likely to be adversely affected by Cu ingestion, but the results of our study do not completely rule out the potential for toxicity in species that might retain Cu fragments for a longer time.

Archives of Environmental Contamination and Toxico↗
USGS2011

Experimental challenge and pathology of highly pathogenic avian influenza virus H5N1 in dunlin ( Calidris alpina ), an intercontinental migrant shorebird species

Background Shorebirds (Charadriiformes) are considered one of the primary reservoirs of avian influenza. Because these species are highly migratory, there is concern that infected shorebirds may be a mechanism by which highly pathogenic avian influenza virus (HPAIV) H5N1 could be introduced into North America from Asia. Large numbers of dunlin ( Calidris alpina ) migrate from wintering areas in central and eastern Asia, where HPAIV H5N1 is endemic, across the Bering Sea to breeding areas in Alaska. Low pathogenic avian influenza virus has been previously detected in dunlin, and thus, dunlin represent a potential risk to transport HPAIV to North America. To date no experimental challenge studies have been performed in shorebirds. Methods Wild dunlin were inoculated intranasally and intrachoanally various doses of HPAIV H5N1. The birds were monitored daily for virus excretion, disease signs, morbidity, and mortality. Results The infectious dose of HPAIV H5N1 in dunlin was determined to be 10 1.7 EID 50 /100 μl and that the lethal dose was 10 1.83 EID 50 /100 μl. Clinical signs were consistent with neurotropic disease, and histochemical analyses revealed that infection was systemic with viral antigen and RNA most consistently found in brain tissues. Infected birds excreted relatively large amounts of virus orally (10 4 EID 50 ) and smaller amounts cloacally. Conclusions Dunlin are highly susceptible to infection with HPAIV H5N1. They become infected after exposure to relatively small doses of the virus and if they become infected, they are most likely to suffer mortality within 3–5 days. These results have important implications regarding the risks of transport and transmission of HPAIV H5N1 to North America by this species and raises questions for further investigation.

Alaska↗
USGS2011

Bat white-nose syndrome in North America

* The newly described fungus, Geomyces destructans, causes an invasive skin infection in bats and is the likely agent of white-nose syndrome (WNS). * With immune system functions and body temperatures reduced during hibernation, bats may be unusually susceptible to a pathogenic fungus such as G. destructans. * WNS was first observed in a popular show cave near Albany, New York, leading some investigators to suspect that a visitor inadvertently introduced G. destructans at this site, triggering a wider WNS outbreak in North America. * Biologists trying to manage WNS within North American bat populations face major challenges, including the variety of susceptible host species, incredible dispersal capabilities of bats, difficulties in treating such populations, and persistence of the pathogen in their vulnerable underground habitats.

Microbe Magazine↗
USGS2011

The population crash of the white-rumped vulture, and its struggle to recover

The white-rumped vulture Gyps bengalensis was once the most abundant bird of prey on the Indian sub-continent. This species easily adapted to life in urban settings; thriving as a keystone species that maintained an ecological balance between the living and the dead. Dead livestock comprised the bulk of the white-rumped vulture diet and was ultimately responsible for its catastrophic population crash. Within ten years of the first documented population declines more than 99% of the white-rumped vultures were lost. The white-rumped vulture was listed as critically endangered in 2000 and has since remained at high risk for extinction.

The Falconer↗
USGS2010

Wing pathology of white-nose syndrome in bats suggests life-threatening disruption of physiology

White-nose syndrome (WNS) is causing unprecedented declines in several species of North American bats. The characteristic lesions of WNS are caused by the fungus Geomyces destructans , which erodes and replaces the living skin of bats while they hibernate. It is unknown how this infection kills the bats. We review here the unique physiological importance of wings to hibernating bats in relation to the damage caused by G. destructans and propose that mortality is caused by catastrophic disruption of wing-dependent physiological functions. Mechanisms of disease associated with G. destructans seem specific to hibernating bats and are most analogous to disease caused by chytrid fungus in amphibians.

BMC Biology↗
USGS2010

Epizootic of beak deformities among wild birds in Alaska: An emerging disease in North America?

The sudden appearance of a large cluster of animals with gross abnormalities may signal a significant change in an ecosystem. We describe an unusual concentration of beak deformities that appear to have arisen rapidly within Alaska and now extend southward along the Pacific Coast. In Alaska we have documented 2,160 Black-capped Chickadees ( Poecile atricapillus ) and 435 individuals of 29 other species of birds, primarily during the past decade, with grossly overgrown and often crossed beaks. The annual prevalence of beak abnormalities among adult Black-capped Chickadees in south-central Alaska varied from 3.6% to 9.7% and averaged 6.5 ± 0.5% between 1999 and 2008. Only 0.05 ± 0.05% of nestlings and 0.3 ± 0.2% of juveniles <6 months old had abnormal beaks, which suggests that this is either a latent developmental or an acquired condition. We documented 80 cases in which a Black-capped Chickadee captured with an apparently normal beak was subsequently recaptured with a beak abnormality and 8 cases in which a beak deformity was no longer detectable upon recapture. Necropsy and histopathology of a sample of affected individuals provided no conclusive evidence of the etiology of this condition. Deformities appear to affect primarily the keratin layer of the beak and may result from abnormally rapid growth of the rhamphotheca. Some affected birds also exhibited lesions in other keratinized tissues of the skin, legs, feet, claws, and feathers, which may represent a systemic disorder or secondary conditions. Additional studies are currently underway to determine diagnostic signs and the underlying cause of this avian keratin disorder.

Alaska↗
USGS2010

Prevalence and pathology of West Nile virus in naturally infected house sparrows, western Nebraska, 2008

Nestling birds are rarely sampled in the field for most arboviruses, yet they may be important in arbovirus amplification cycles. We sampled both nestling and adult house sparrows ( Passer domesticus ) in western Nebraska for West Nile virus (WNV) or WNV-specific antibodies throughout the summer of 2008 and describe pathology in naturally infected nestlings. Across the summer, 4% of nestling house sparrows were WNV-positive; for the month of August alone, 12.3% were positive. Two WNV-positive nestlings exhibited encephalitis, splenomegaly, hepatic necrosis, nephrosis, and myocarditis. One nestling sparrow had large mural thrombi in the atria and ventricle and immunohistochemical staining of WNV antigen in multiple organs including the wall of the aorta and pulmonary artery; cardiac insufficiency thus may have been a cause of death. Adult house sparrows showed an overall seroprevalence of 13.8% that did not change significantly across the summer months. The WNV-positive nestlings and the majority of seropositive adults were detected within separate spatial clusters. Nestling birds, especially those reared late in the summer when WNV activity is typically greatest, may be important in virus amplification.

Nebraska↗
USGS2010

Pathology and virus detection in tissues of nestling house sparrows naturally infected with Buggy Creek virus (Togaviridae).

Alphaviruses ( Togaviridae ) infect wild birds, but clinical illness and death attributable to virus in naturally infected birds is rarely reported, particularly for small passerine species or nestlings. Buggy Creek virus is a unique alphavirus in the Western equine encephalomyelitis virus (WEEV) complex that is vectored by the cimicid swallow bug ( Oeciacus vicarius ), an ectoparasite of the colonially nesting Cliff Swallow ( Petrochelidon pyrrhonota ) and the introduced House Sparrow ( Passer domesticus ). While sampling birds for Buggy Creek virus (BCRV) during the summers of 2007 and 2008, we discovered large numbers of clinically ill or dead House Sparrow nestlings. Ill nestlings exhibited ataxia, torticollis, paresis, and lethargy. Histologic examination revealed that encephalitis was the most common finding, followed by myositis, myocarditis, and hepatic changes, but pathology was highly variable. We isolated BCRV from brain tissue in most of the ill or dead nestlings, and from blood, liver, kidney, spleen, lung, feather pulp, and skin in some birds. To our knowledge, this is the first report of clinical illness, gross pathology, and histopathology for a WEEV-complex alphavirus in a field-collected passerine species.

Journal of Wildlife Diseases↗
USGS2009

Comparison of monkeypox viruses pathogenesis in mice by in vivo imaging

Monkeypox viruses (MPXV) cause human monkeypox, a zoonotic smallpox-like disease endemic to Africa, and are of worldwide public health and biodefense concern. Using viruses from the Congo (MPXV-2003-Congo-358) and West African (MPXV-2003-USA-044) clades, we constructed recombinant viruses that express the luciferase gene (MPXV-Congo/Luc+and MPXV-USA-Luc+) and compared their viral infection in mice by biophotonic imaging. BALB/c mice became infected by both MPXV clades, but they recovered and cleared the infection within 10 days post-infection (PI). However, infection in severe combined immune deficient (SCID) BALB/c mice resulted in 100% lethality. Intraperitoneal (IP) injection of both MPXV-Congo and MPXV-Congo/Luc+resulted in a systemic clinical disease and the same mean time-to-death at 9 (??0) days post-infection. Likewise, IP injection of SCID-BALB/c mice with MPXV-USA or the MPXV-USA-Luc+, resulted in similar disease but longer (P<0.05) mean time-to-death (11??0 days) for both viruses compared to the Congo strains. Imaging studies in SCID mice showed luminescence in the abdomen within 24 hours PI with subsequent spread elsewhere. Animals infected with the MPXV-USA/Luc+had less intense luminescence in tissues than those inoculated with MPXV-Congo/Luc+, and systemic spread of the MPXV-USA/Luc+virus occurred approximately two days later than the MPXV-Congo/Luc+. The ovary was an important target for viral replication as evidenced by the high viral titers and immunohistochemistry. These studies demonstrate the suitability of a mouse model and biophotonic imaging to compare the disease progression and tissue tropism of MPX viruses.

PLoS ONE↗
USGS2009

Histopathologic criteria to confirm white-nose syndrome in bats

White-nose syndrome (WNS) is a cutaneous fungal disease of hibernating bats associated with a novel Geomyces sp. fungus. Currently, confirmation of WNS requires histopathologic examination. Invasion of living tissue distinguishes this fungal infection from those caused by conventional transmissible dermatophytes. Although fungal hyphae penetrate the connective tissue of glabrous skin and muzzle, there is typically no cellular inflammatory response in hibernating bats. Preferred tissue samples to diagnose this fungal infection are rostral muzzle with nose and wing membrane fixed in 10% neutral buffered formalin. To optimize detection, the muzzle is trimmed longitudinally, the wing membrane is rolled, and multiple cross-sections are embedded to increase the surface area examined. Periodic acid-Schiff stain is essential to discriminate the nonpigmented fungal hyphae and conidia. Fungal hyphae form cup-like epidermal erosions and ulcers in the wing membrane and pinna with involvement of underlying connective tissue. In addition, fungal hyphae are present in hair follicles and in sebaceous and apocrine glands of the muzzle with invasion of tissue surrounding adnexa. Fungal hyphae in tissues are branching and septate, but the diameter and shape of the hyphae may vary from parallel walls measuring 2 ??m in diameter to irregular walls measuring 3-5 ??m in diameter. When present on short aerial hyphae, curved conidia are approximately 2.5 ??m wide and 7.5 ??m in curved length. Conidia have a more deeply basophilic center, and one or both ends are usually blunt. Although WNS is a disease of hibernating bats, severe wing damage due to fungal hyphae may be seen in bats that have recently emerged from hibernation. These recently emerged bats also have a robust suppurative inflammatory response.

Journal of Veterinary Diagnostic Investigation↗
USGS2008

Mortality of ducklings of the black-bellied whistling duck (Dendrocygna autumnalis) during their premier swim in a hypersaline lake in south Texas

Adult black-bellied whistling ducks ( Dendrocygna autumnalis ) were observed leaving islands with recently hatched young in a South Texas hypersaline lake during summer 2003. We counted 216 ducklings from 20 broods attempting to make their first swim to the mainland, presumably heading for suitable rearing habitat. Of these, 144 (67%) either died in the water or on the salt-encrusted shoreline within minutes to a few hours of first entering the water. An additional 35 carcasses from unobserved broods were found. Nine carcasses of ducklings were necropsied and they had levels of sodium in the brain above the lethal threshold concentration for sodium poisoning. From our surveillance efforts, we documented a decrease in maximum number of adult black-bellied whistling ducks observed on the islands from 489 in 2002 to 138 in 2003.

South Texas↗
USGS2005

Attempts to identify the source of avian vacuolar myelinopathy for waterbirds

Attempts were made to reproduce avian vacuolar myelinopathy (AVM) in a number of test animals in order to determine the source of the causative agent for birds and to find a suitable animal model for future studies. Submerged vegetation, plankton, invertebrates, forage fish, and sediments were collected from three lakes with ongoing outbreaks of AVM and fed to American coots ( Fulica americana ), mallard ducks and ducklings ( Anas platyrhynchos ), quail ( Coturnix japonica ), and laboratory mice either via gavage or ad libitum. Tissues from AVM-affected coots with brain lesions were fed to ducklings, kestrels ( Falco sparverius ), and American crows ( Corvus brachyrhynchos ). Two mallards that ingested one sample of Hydrilla verticillata along with any biotic or abiotic material associated with its external surface developed brain lesions consistent with AVM, although neither of the ducks had clinical signs of disease. Ingestion of numerous other samples of Hydrilla from the AVM affected lakes and a lake with no prior history of AVM, other materials (sediments, algae, fish, invertebrates, and water from affected lakes), or tissues from AVM-affected birds did not produce either clinical signs or brain lesions in any of the other test animals in our studies. These results suggest that waterbirds are most likely exposed to the causative agent of AVM while feeding on aquatic vegetation, but we do not believe the vegetation itself is the agent. We hypothesize that the causative agent of AVM might either be accumulated by aquatic vegetation, such as Hydrilla , or associated with biotic or abiotic material on its external surfaces. In support of that hypothesis, two coots that ingested Hydrilla sampled from a lake with an ongoing AVM outbreak in wild birds developed neurologic signs within 9 days (ataxia, limb weakness, and incoordination), and one of two coots that ingested Hydrilla collected from the same site 13 days later became sick and died within 38 days. None of these three sick coots had definitive brain lesions consistent with AVM by light microscopy, but they had no gross or histologic lesions in other tissues. It is unclear if these birds died of AVM. Perhaps they did not ingest a dose sufficient to produce brain lesions or the lesions were ultrastructural. Alternatively, it is possible that a separate neurotoxic agent is responsible for the morbidity and mortality observed in these coots.

Journal of Wildlife Diseases↗
USGS2005

Coral disease and health workshop: Coral histopathology II, July 12-14, 2005

The health and continued existence of coral reef ecosystems are threatened by an increasing array of environmental and anthropogenic impacts. Coral disease is one of the prominent causes of increased mortality among reefs globally, particularly in the Caribbean. Although over 40 different coral diseases and syndromes have been reported worldwide, only a few etiological agents have been confirmed; most pathogens remain unknown and the dynamics of disease transmission, pathogenicity and mortality are not understood. Causal relationships have been documented for only a few of the coral diseases, while new syndromes continue to emerge. Extensive field observations by coral biologists have provided substantial documentation of a plethora of new pathologies, but our understanding, however, has been limited to descriptions of gross lesions with names reflecting these observations (e.g., black band, white band, dark spot). To determine etiology, we must equip coral diseases scientists with basic biomedical knowledge and specialized training in areas such as histology, cell biology and pathology. Only through combining descriptive science with mechanistic science and employing the synthesis epizootiology provides will we be able to gain insight into causation and become equipped to handle the pending crisis. One of the critical challenges faced by coral disease researchers is to establish a framework to systematically study coral pathologies drawing from the field of diagnostic medicine and pathology and using generally accepted nomenclature. This process began in April 2004, with a workshop titled Coral Disease and Health Workshop: Developing Diagnostic Criteria co-convened by the Coral Disease and Health Consortium (CDHC), a working group organized under the auspices of the U.S. Coral Reef Task Force, and the International Registry for Coral Pathology (IRCP). The workshop was hosted by the U.S. Geological Survey, National Wildlife Health Center (NWHC) in Madison, Wisconsin and was focused on gross morphology and disease signs observed in the field. A resounding recommendation from the histopathologists participating in the workshop was the urgent need to develop diagnostic criteria that are suitable to move from gross observations to morphological diagnoses based on evaluation of microscopic anatomy. As a continuation of building the foundation and framework for coral disease diagnostics, the CDHC convened the Coral Disease and Health Workshop: Coral Histopathology II in Charleston, South Carolina, July 11-14, 2005. The workshop was hosted by the Department of Pathology and Laboratory Medicine at the Medical University of South Carolina, Charleston, SC which provided expertise, facilities and equipment in support of the workshop. All of the histological slides and related photographs used in the discussions were prepared and supplied by the IRCP. This workshop brought together 15 experts in veterinary and medical pathology and coral biology from national and international research institutes and government laboratories. The mission was to devise a standardized approach to examining microscopic anatomy and pathology of corals and a standardized nomenclature to facilitate accurate descriptions of the microscopic morphology of corals and enhance communication among specialists investigating causes of coral death. 2 The participants of this workshop deliberated for 3 days to refine the nomenclature for gross and microscopic anatomy of corals and systematically described microscopic changes associated with selected coral diseases. The findings and recommendations from the deliberations will be submitted to the research community for peer review. The standardized nomenclature and descriptions produced at this workshop will ultimately be made available to the scientific community through a variety of media including the World Wide Web. An exciting highlight of this meeting was provided by Professor Robert Ogilvie (MUSC Department of Cell Biology and Anatomy) when he introduced participants to a new digital technology that is revolutionizing histology and histopathology in the medical field. The Virtual Slide technology creates digital images of histological tissue sections by computer scanning actual slides in high definition and storing the images for retrieval and viewing. Virtual slides now allow any investigator with access to a computer and the web to view, search, annotate and comment on the same tissue sections in real time. Medical and veterinary slide libraries across the country are being converted into virtual slides to enhance biomedical education, research and diagnosis. The coral health and disease researchers at this workshop deem virtual slides as a significant way to increase capabilities in coral histology and a means for pathology consultations on coral disease cases on a global scale.

NOAA Technical Memorandum↗
USGS2004

Mortality in Laysan ducks (Anas laysanensis) by emaciation complicated by Echinuria uncinata on Laysan Island, Hawaii, 1993

In November 1993, unusual mortality occurred among endangered Laysan ducks on Laysan Island, one of the remote refugia of the Northwestern Hawaiian Islands National Wildlife Refuge (USA). Ten live ducks were emaciated, and blood samples documented anemia, heterophilia, and eosinophilia. Pathology in 13 duck carcasses revealed emaciation, marked thickening of the proventricular wall, abundant mucus, and nodules in the gastrointestinal tract. Histology revealed granulomata associated with nematodes in the proventriculus, small intestines, and body walls of nine of 10 ducks examined on histology. We suspect that low rainfall and low food abundance that year contributed to enhanced pathogenicity of parasite infection, either through increased exposure or decreased host resistance. Because the Laysan duck is found only on Laysan island and is critically endangered, translocation of this species to other islands is being considered. Given that we have not seen pathology associated with Echinuria spp. in native waterfowl on other Hawaiian Islands and given the parasite's potential to cause significant lesions in Laysan ducks, it will be important to prevent the translocation of Echinuria spp.

Hawai'i↗