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Geology topics

C.U. Meteyer

Publications and source records attributed to C.U. Meteyer.

13 recordsLinked to original sources
USGS2011

Experimental infection of bats with Geomyces destructans causes white-nose syndrome

White-nose syndrome (WNS) has caused recent catastrophic declines among multiple species of bats in eastern North America. The disease's name derives from a visually apparent white growth of the newly discovered fungus Geomyces destructans on the skin (including the muzzle) of hibernating bats. Colonization of skin by this fungus is associated with characteristic cutaneous lesions that are the only consistent pathological finding related to WNS. However, the role of G. destructans in WNS remains controversial because evidence to implicate the fungus as the primary cause of this disease is lacking. The debate is fuelled, in part, by the assumption that fungal infections in mammals are most commonly associated with immune system dysfunction. Additionally, the recent discovery that G. destructans commonly colonizes the skin of bats of Europe, where no unusual bat mortality events have been reported, has generated further speculation that the fungus is an opportunistic pathogen and that other unidentified factors are the primary cause of WNS. Here we demonstrate that exposure of healthy little brown bats (Myotis lucifugus) to pure cultures of G. destructans causes WNS. Live G. destructans was subsequently cultured from diseased bats, successfully fulfilling established criteria for the determination of G. destructans as a primary pathogen. We also confirmed that WNS can be transmitted from infected bats to healthy bats through direct contact. Our results provide the first direct evidence that G. destructans is the causal agent of WNS and that the recent emergence of WNS in North America may represent translocation of the fungus to a region with a naive population of animals. Demonstration of causality is an instrumental step in elucidating the pathogenesis and epidemiology of WNS and in guiding management actions to preserve bat populations against the novel threat posed by this devastating infectious disease. ?? 2011 Macmillan Publishers Limited. All rights reserved.

Nature↗
USGS2009

Bat white-nose syndrome: An emerging fungal pathogen?

White-nose syndrome (WNS) is a condition associated with an unprecedented bat mortality event in the northeastern United States. Since the winter of 2006*2007, bat declines exceeding 75% have been observed at surveyed hibernacula. Affected bats often present with visually striking white fungal growth on their muzzles, ears, and/or wing membranes. Direct microscopy and culture analyses demonstrated that the skin of WNS-affected bats is colonized by a psychro-philic fungus that is phylogenetically related to Geomyces spp. but with a conidial morphology distinct from characterized members of this genus. This report characterizes the cutaneous fungal infection associated with WNS.

Northeast↗
USGS2008

Apparent tolerance of turkey vultures (Cathartes aura) to the non-steroidal anti-inflammatory drug diclofenac

The nonsteroidal anti‐inflammatory drug diclofenac is extremely toxic to Old World Gyps vultures (median lethal dose ∼0.1–0.2 mg/kg), evoking visceral gout, renal necrosis, and mortality within a few days of exposure. Unintentional secondary poisoning of vultures that fed upon carcasses of diclofenac‐treated livestock decimated populations in the Indian subcontinent. Because of the widespread use of diclofenac and other cyclooxygenase‐2 inhibiting drugs, a toxicological study was undertaken in turkey vultures ( Cathartes aura ) as an initial step in examining sensitivity of New World scavenging birds. Two trials were conducted entailing oral gavage of diclofenac at doses ranging from 0.08 to 25 mg/kg body weight. Birds were observed for 7 d, blood samples were collected for plasma chemistry (predose and 12, 24, and 48 h and 7 d postdose), and select individuals were necropsied. Diclofenac failed to evoke overt signs of toxicity, visceral gout, renal necrosis, or elevate plasma uric acid at concentrations greater than 100 times the estimated median lethal dose reported for Gyps vultures. For turkey vultures receiving 8 or 25 mg/kg, the plasma half‐life of diclofenac was estimated to be 6 h, and it was apparently cleared after several days as no residues were detectable in liver or kidney at necropsy. Differential sensitivity among avian species is a hallmark of cyclooxygenase‐2 inhibitors, and despite the tolerance of turkey vultures to diclofenac, additional studies in related scavenging species seem warranted.

Environmental Toxicology and Chemistry↗
USGS2007

Protozoal meningoencephalitis in sea otters (Enhydra lutris): A histopathological and immunohistochemical study of naturally occurring cases

Protozoal meningoencephalitis is considered to be an important cause of mortality in the California sea otter ( Enhydra lutris ). Thirty nine of 344 (11.3%) California (CA) and Washington state (WA) sea otters examined from 1985 to 2004 had histopathological evidence of significant protozoal meningoencephalitis. The aetiological agents and histopathological changes associated with these protozoal infections are described. The morphology of the actively multiplicative life stages of the organisms (tachyzoites for Toxoplasma gondii and merozoites for Sarcocystis neurona ) and immunohistochemical labelling were used to identify infection with S. neurona ( n =22, 56.4%), T. gondii ( n =5, 12.8%) or dual infection with both organisms ( n =12, 30.8%). Active S. neurona was present in all dual infections, while most had only the latent form of T. gondii . In S. neurona meningoencephalitis, multifocal to diffuse gliosis was widespread in grey matter and consistently present in the molecular layer of the cerebellum. In T. gondii meningoencephalitis, discrete foci of gliosis and malacia were more widely separated, sometimes incorporated pigment-laden macrophages and mineral, and were found predominantly in the cerebral cortex. Quiescent tissue cysts of T. gondii were considered to be incidental and not a cause of clinical disease and mortality. Protozoal meningoencephalitis was diagnosed more frequently in the expanding population of WA sea otters (10 of 31, 32.3%) than in the declining CA population (29 of 313, 9.3%). Among sea otters with protozoal meningoencephalitis, those that had displayed neurological signs prior to death had active S. neurona encephalitis, supporting the conclusion that S. neurona is the most significant protozoal pathogen in the central nervous system of sea otters.

California, Washington↗
USGS2007

Raptor mortality due to West Nile virus in the United States, 2002

West Nile virus (WNV) has affected many thousands of birds since it was first detected in North America in 1999, but the overall impact on wild bird populations is unknown. In mid-August 2002, wildlife rehabilitators and local wildlife officials from multiple states began reporting increasing numbers of sick and dying raptors, mostly red-tailed hawks ( Buteo jamaicensis ) and great horned owls ( Bubo virginianus) . Commonly reported clinical signs were nonspecific and included emaciation, lethargy, weakness, inability to perch, fly or stand, and nonresponse to danger. Raptor carcasses from 12 states were received, and diagnostic evaluation of 56 raptors implicated WNV infection in 40 (71%) of these cases. Histologically, nonsuppurative encephalitis and myocarditis were the salient lesions (79% and 61%, respectively). Other causes of death included lead poisoning, trauma, aspergillosis, and Salmonella spp. and Clostridium spp. infections. The reason(s) for the reported increase in raptor mortality due to WNV in 2002 compared with the previous WNV seasons is unclear, and a better understanding of the epizootiology and pathogenesis of the virus in raptor populations is needed.

Journal of Wildlife Diseases↗
USGS2004

Diclofenac residues as the cause of vulture population decline in Pakistan

The Oriental white-backed vulture (OWBV; Gyps bengalensis ) was once one of the most common raptors in the Indian subcontinent 1 . A population decline of >95%, starting in the 1990s, was first noted at Keoladeo National Park, India 2 . Since then, catastrophic declines, also involving Gyps indicus and Gyps tenuirostris , have continued to be reported across the subcontinent 3 . Consequently these vultures are now listed as critically endangered by BirdLife International 4 . In 2000, the Peregrine Fund initiated its Asian Vulture Crisis Project with the Ornithological Society of Pakistan, establishing study sites at 16 OWBV colonies in the Kasur, Khanewal and Muzaffargarh–Layyah Districts of Pakistan to measure mortality at over 2,400 active nest sites 5 . Between 2000 and 2003, high annual adult and subadult mortality (5–86%) and resulting population declines (34–95%) (ref. 5 and M.G., manuscript in preparation) were associated with renal failure and visceral gout. Here, we provide results that directly correlate residues of the anti-inflammatory drug diclofenac with renal failure. Diclofenac residues and renal disease were reproduced experimentally in OWBVs by direct oral exposure and through feeding vultures diclofenac-treated livestock. We propose that residues of veterinary diclofenac are responsible for the OWBV decline.

Nature↗
USGS2004

Investigations of a large scale eared grebe (Podiceps nigricollis) die-off at the Salton Sea, California in 1992

An estimated 150,000 Eared Grebes (Podiceps nigricollis) died at the Salton Sea between 16 December 1991 and 21 April 1992. This represented the largest documented mortality event of Eared Grebes at the time and approximately 6% of the North American population. During the die-off, grebes exhibited several uncharacteristic behaviors, such as congregating at freshwater tributaries, repeatedly gulping freshwater, preening excessively, moving onto land, and allowing close approach and/or capture. Avian cholera was diagnosed in Eared Grebes collected along the north and west shoreline of the Sea late in the die-off but not from the majority of the Eared Grebes dying along the south shore. Gross and histological examinations and diagnostic testing for viruses, bacteria, and parasites did not identify the cause of mortality in the majority of Eared Grebes examined from the south shore of the Sea. Liver concentrations of arsenic, chromium, DDE, mercury, selenium, and zinc were elevated in some Eared Grebes, but none of those contaminants exceeded known thresholds for independent lethality. Poisoning by heavy metals, organochlorine, organophosphorus, or carbamate pesticides, avian botulism, and salt were ruled out as the cause of mortality. Hypotheses for the die-off are interactive effects of contaminants, immunosuppression, a yet unidentified biotoxin or pathogen present in the Salton Sea, impairment of feather waterproofing leading to hypothermia, or a unique manifestation of avian cholera that evades laboratory detection.

California↗
USGS2001

Lead poisoning of waterfowl by contaminated sediment in the Coeur D'Alene River

The Coeur d'Alene River basin in Idaho has been contaminated by mine tailings that have impaired the health of wildlife since the early 1900s. In other parts of the world, virtually all lead poisoning of waterfowl is caused by the ingestion of manmade lead artifacts, primarily spent lead shotshell pellets or, occasionally, fishing sinkers. However, in the Coeur d'Alene River basin in Idaho, nonartifactual lead poisoning was the ultimate cause of death of most of 219 (77%) of 285 waterfowl carcasses that had been found sick or dead from 1992 through 1997. The majority of these 219 waterfowl (172 tundra swans [Cygnus columbianus], 33 Canada geese [Branta canadensis], and 14 other species) were poisoned by ingesting river sediment that was contaminated with lead. The next most common cause of death (20 instances, 7%) was lead poisoning accompanied by ingested shotshell pellets. The remaining 46 waterfowl succumbed to trauma, infectious diseases (aspergillosis, avian cholera, tuberculosis), or miscellaneous problems, or the cause of death was not determined.

Idaho↗
USGS2001

Leaping lopsided: a review of the current hypotheses regarding etiologies of limb malformations in frogs

Recent progress in the investigation of limb malformations in free-living frogs has underlined the wide range in the types of limb malformations and the apparent spatiotemporal clustering of their occurrence. Here, we review the current understanding of normal and abnormal vertebrate limb development and regeneration and discuss some of the molecular events that may bring about limb malformation. Consideration of the differences between limb development and regeneration in amphibians has led us to the hypothesis that some of the observed limb malformations come about through misdirected regeneration. We report the results of a pilot study that supports this hypothesis. In this study, the distal aspect of the right hindlimb buds of X. laevis tadpoles was amputated at the pre-foot paddle stage. The tadpoles were raised in water from a pond in Minnesota at which 7% of surveyed newly metamorphosed feral frogs had malformations. Six percent (6 of 100) of the right limbs of the tadpoles raised in pond water developed abnormally. One truncated right limb was the only malformation in the control group, which was raised in dechlorinated municipal water. All unamputated limbs developed normally in both groups. Three major factors under consideration for effecting the limb malformations are discussed. These factors include environmental chemicals (primarily agrichemicals), encysted larvae (metacercariae) of trematode parasites, and increased levels of ultraviolet light. Emphasis is placed on the necessary intersection of environmental stressors and developmental events to bring about the specific malformations that are observed in free-living frog populations.

California, Maine, Minnesota, Quebec, Vermont↗
USGS2000

Hind limb malformations in free-living northern leopard frogs (Rana pipiens) from Maine, Minnesota, and Vermont suggest multiple etiologies

Background Reports of malformed frogs have increased throughout the North American continent in recent years. Most of the observed malformations have involved the hind limbs. The goal of this study was to accurately characterize the hind limb malformations in wild frogs as an important step toward understanding the possible etiologies. Methods During 1997 and 1998, 182 recently metamorphosed northern leopard frogs (Rana pipiens) were collected from Minnesota, Vermont, and Maine. Malformed hind limbs were present in 157 (86%) of these frogs, which underwent necropsy and radiographic evaluation at the National Wildlife Health Center. These malformations are described in detail and classified into four major categories: (1) no limb (amelia); (2) multiple limbs or limb elements (polymelia, polydactyly, polyphalangy); (3) reduced limb segments or elements (phocomelia, ectromelia, ectrodactyly, and brachydactyly; and (4) distally complete but malformed limb (bone rotations, bridging, skin webbing, and micromelia). Results Amelia and reduced segments and/or elements were the most common finding. Frogs with bilateral hind limb malformations were not common, and in only eight of these 22 frogs were the malformations symmetrical. Malformations of a given type tended to occur in frogs collected from the same site, but the types of malformations varied widely among all three states, and between study sites within Minnesota. Conclusions Clustering of malformation type suggests that developmental events may produce a variety of phenotypes depending on the timing, sequence, and severity of the environmental insult. Hind limb malformations in free-living frogs transcend current mechanistic explanations of tetrapod limb development.

Maine, Minnesota, Vermont↗
USGS2000

Defining anural malformations in the context of a developmental problem

This paper summarizes terminology and general concepts involved in animal development for the purpose of providing background for the study and understanding of frog malformations. The results of our radiographic investigation of rear limb malformations in Rana pipiens provide evidence that frog malformations are the product of early developmental errors. Although bacteria, parasites and viruses were identified in these metamorphosed frogs, the relevant window to look for the teratogenic effect of these agents is in the early tadpole stage during limb development. As a result, our microbiological findings must be regarded as inconclusive relative to determining their contribution to malformations because we conducted our examinations on metamorphosed frogs not tadpoles. Future studies need to look at teratogenic agents (chemical, microbial, physical or mechanical) that are present in the embryo, tadpole, and their environments at the stages of development that are relevant for the malformation type. The impact of these teratogenic agents then needs to be assessed in appropriate animal models using studies that are designed to mimic field conditions. The results of these laboratory tests should then be analyzed in such a way that will allow comparison with the findings in the wild-caught tadpoles and frogs.

Journal of the Iowa Academy of Science↗
USGS1998

Epizootic vacuolar myelinopathy of the central nervous system of bald eagles ( Haliaeetus leucocephalus ) and American coots ( Fulica americana )

Unprecedented mortality occurred in bald eagles ( Haliaeetus leucocephalus ) at DeGray Lake, Arkansas, during the winters of 1994-1995 and 1996-1997. The first eagles were found dead during November, soon after arrival from fall migration, and deaths continued into January during both episodes. In total, 29 eagles died at or near DeGray Lake in the winter of 1994-1995 and 26 died in the winter of 1996-1997; no eagle mortality was noted during the same months of the intervening winter or in the earlier history of the lake. During the mortality events, sick eagles were observed overflying perches or colliding with rock walls. Signs of incoordination and limb paresis were also observed in American coots ( Fulica americana ) during the episodes of eagle mortality, but mortality in coots was minimal. No consistent abnormalities were seen on gross necropsy of either species. No microscopic findings in organs other than the central nervous system (CNS) could explain the cause of death. By light microscopy, all 26 eagles examined and 62/77 (81%) coots had striking, diffuse, spongy degeneration of the white matter of the CNS. Vacuolation occurred in all myelinated CNS tissue, including the cerebellar folia and medulla oblongata, but was most prominent in the optic tectum. In the spinal cord, vacuoles were concentrated near the gray matter, and occasional swollen axons were seen. Vacuoles were uniformly present in optic nerves but were not evident in the retina or peripheral or autonomic nerves. Cellular inflammatory response to the lesion was distinctly lacking. Vacuoles were 8-50 microns in diameter and occurred individually, in clusters, or in rows. In sections stained by luxol fast blue/periodic acid-Schiff stain, the vacuoles were delimited and transected by myelin strands. Transmission electron microscopy revealed intramyelinic vacuoles formed in the myelin sheaths by splitting of one or more myelin lamellae at the intraperiodic line. This lesion is characteristic of toxicity from hexachlorophene, triethyltin, bromethalin, isonicotinic acid hydrazide, and certain exotic plant toxins; however, despite exhaustive testing, no etiology was determined for the DeGray Lake mortality events. This is the first report of vacuolar myelinopathy associated with spontaneous mortality in wild birds.

Arkansas↗