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Carol U. Meteyer

Publications and source records attributed to Carol U. Meteyer.

At least 19 recordsLinked to original sources
USGS2018

Information to prevent human exposure to disease agents associated with wildlife—U.S. Geological Survey circulars on zoonotic disease

The U.S. Geological Survey in collaboration with the U.S. Fish and Wildlife Service and others have published reports with information about geographic distribution, specific pathogens, disease ecology, and strategies to avoid exposure and infection for a selection of zoonotic diseases. Zoonotic diseases are diseases that can be passed from animals to humans, such as rabies and plague. This summary factsheet highlights the reports on plague, bat rabies, and raccoon roundworm with links to all seven zoonotic diseases covered in this series.

Fact Sheet↗
USGS2018

Experimental infection of Tadarida brasiliensis with Pseudogymnoascus destructans, the fungus that causes white-nose syndrome

White-nose syndrome (WNS) is causing significant declines in populations of North American hibernating bats, and recent western and southern expansions of the disease have placed additional species at risk. Understanding differences in species susceptibility and identifying management actions to reduce mortality of bats from WNS are top research priorities. However, the use of wild-caught susceptible bats, such as Myotis lucifugus , as model species for WNS research is problematic and places additional pressure on remnant populations. We investigated the feasibility of using Tadarida brasiliensis , a highly abundant species of bat that tolerates captivity, as the basis for an experimental animal model for WNS. Using methods previously established to confirm the etiology of WNS in M. lucifugus , we experimentally infected 11 T. brasiliensis bats with Pseudogymnoascus destructans in the laboratory under conditions that induced hibernation. We detected P. destructans on all 11 experimentally infected bats, 7 of which exhibited localized proliferation of hyphae within the epidermis, dermis, and subcutaneous tissue, similar to invasive cutaneous ascomycosis observed in M. lucifugus bats with WNS. However, the distribution of lesions across wing membranes of T. brasiliensis bats was limited, and only one discrete “cupping erosion,” diagnostic for WNS, was identified. Thus, the rarity of lesions definitive for WNS suggests that T. brasiliensis does not likely represent an appropriate model for studying the pathophysiology of this disease. Nonetheless, the results of this study prompt questions concerning the potential for free-ranging, migratory T. brasiliensis bats to become infected with P. destructans and move the fungal pathogen between roost sites used by species susceptible to WNS.

mSphere↗
USGS2016

Bald Eagle nestling mortality associated with Argas radiatus and Argas ricei tick infestation and successful management with nest removal in Arizona, USA

Eight Bald Eagle ( Haliaeetus leucocephalus ) nestlings heavily infested with larval ticks were found in or under a nest near the confluence of the Verde and Salt rivers in Arizona in 2009-11. The 8-12-wk-old nestlings were slow to respond to stimuli and exhibited generalized muscle weakness or paresis of the pelvic limbs. Numerous cutaneous and subcutaneous hemorrhages were associated with sites of tick attachment. Ticks were identified as Argas radiatus and Argas ricei . Treatment with acaricides and infection with West Nile virus (WNV) may have confounded the clinical presentation in 2009 and 2010. However, WNV-negative birds exhibited similar signs in 2011. One nestling recovered from paresis within 36 h after the removal of all adult and larval ticks (>350) and was released within 3 wk. The signs present in the heavily infested Bald Eagle nestlings resembled signs associated with tick paralysis, a neurotoxin-mediated paralytic syndrome described in mammals, reptiles, and wild birds (though not eagles). Removal of the infested nest and construction of a nest platform in a different tree was necessary to break the cycle of infection. The original nesting pair constructed a new nest on the man-made platform and successfully fledged two Bald Eagles in 2012.

Arizona↗
USGS2014

White-nose syndrome initiates a cascade of physiologic disturbances in the hibernating bat host

Background The physiological effects of white-nose syndrome (WNS) in hibernating bats and ultimate causes of mortality from infection with Pseudogymnoascus (formerly Geomyces ) destructans are not fully understood. Increased frequency of arousal from torpor described among hibernating bats with late-stage WNS is thought to accelerate depletion of fat reserves, but the physiological mechanisms that lead to these alterations in hibernation behavior have not been elucidated. We used the doubly labeled water (DLW) method and clinical chemistry to evaluate energy use, body composition changes, and blood chemistry perturbations in hibernating little brown bats ( Myotis lucifugus ) experimentally infected with P. destructans to better understand the physiological processes that underlie mortality from WNS. Results These data indicated that fat energy utilization, as demonstrated by changes in body composition, was two-fold higher for bats with WNS compared to negative controls. These differences were apparent in early stages of infection when torpor-arousal patterns were equivalent between infected and non-infected animals, suggesting that P. destructans has complex physiological impacts on its host prior to onset of clinical signs indicative of late-stage infections. Additionally, bats with mild to moderate skin lesions associated with early-stage WNS demonstrated a chronic respiratory acidosis characterized by significantly elevated dissolved carbon dioxide, acidemia, and elevated bicarbonate. Potassium concentrations were also significantly higher among infected bats, but sodium, chloride, and other hydration parameters were equivalent to controls. Conclusions Integrating these novel findings on the physiological changes that occur in early-stage WNS with those previously documented in late-stage infections, we propose a multi-stage disease progression model that mechanistically describes the pathologic and physiologic effects underlying mortality of WNS in hibernating bats. This model identifies testable hypotheses for better understanding this disease, knowledge that will be critical for defining effective disease mitigation strategies aimed at reducing morbidity and mortality that results from WNS.

BMC Physiology↗
USGS2014

Pathology in euthermic bats with white nose syndrome suggests a natural manifestation of immune reconstitution inflammatory syndrome

White nose syndrome, caused by Geomyces destructans, has killed more than 5 million cave hibernating bats in eastern North America. During hibernation, the lack of inflammatory cell recruitment at the site of fungal infection and erosion is consistent with a temperature-induced inhibition of immune cell trafficking. This immune suppression allows G. destructans to colonize and erode the skin of wings, ears and muzzle of bat hosts unchecked. Yet, paradoxically, within weeks of emergence from hibernation an intense neutrophilic inflammatory response to G. destructans is generated, causing severe pathology that can contribute to death. We hypothesize that the sudden reversal of immune suppression in bats upon the return to euthermia leads to a form of immune reconstitution inflammatory syndrome (IRIS), which was first described in HIV-infected humans with low helper T lymphocyte counts and bacterial or fungal opportunistic infections. IRIS is a paradoxical and rapid worsening of symptoms in immune compromised humans upon restoration of immunity in the face of an ongoing infectious process. In humans with HIV, the restoration of adaptive immunity following suppression of HIV replication with anti-retroviral therapy (ART) can trigger severe immune-mediated tissue damage that can result in death. We propose that the sudden restoration of immune responses in bats infected with G. destructans results in an IRIS-like dysregulated immune response that causes the post-emergent pathology.

Virulence↗
USGS2014

Lapland longspur mortality at an oil well drilling rig site, Laramie County, Wyoming

Two hundred fifty-one Lapland longspur ( Calcarius lapponicus ) carcasses were recovered around an oil well drilling rig in Laramie County, Wyoming, USA, on December 13–14, 2010, apparent victims of a winter storm and “light entrapment” from the lights on the drilling rig during foggy conditions. We found Lapland longspur carcasses distributed around the drilling rig from 33 m to 171 m. Investigators did not find evidence of bird carcasses on the drilling rig deck or equipment immediately adjacent to the drilling rig. We ruled out chemical toxins and disease as a cause of mortality. Weather conditions, the circular depositional pattern of carcasses around the drilling rig, and bird necropsy results led investigators to conclude that the Lapland longspur mortality was the result of the migrating birds entering the area illuminated by the drilling rig lights in freezing fog and the birds repeatedly circling the drilling rig until they fell to the ground in exhaustion and dying from subsequent trauma. Further research is needed to understand how to most effectively adjust lighting of onshore drilling rigs to reduce the potential for avian light entrapment. Published 2014. This article is a U.S. Government work and is in the public domain in the USA.

Wyoming↗
USGS2014

To understand coral disease, look at coral cells

Diseases threaten corals globally, but 40 years on their causes remain mostly unknown. We hypothesize that inconsistent application of a complete diagnostic approach to coral disease has contributed to this slow progress. We quantified methods used to investigate coral disease in 492 papers published between 1965 and 2013. Field surveys were used in 65% of the papers, followed by biodetection (43%), laboratory trials (20%), microscopic pathology (21%), and field trials (9%). Of the microscopic pathology efforts, 57% involved standard histopathology at the light microscopic level (12% of the total investigations), with the remainder dedicated to electron or fluorescence microscopy. Most (74%) biodetection efforts focused on culture or molecular characterization of bacteria or fungi from corals. Molecular and immunological tools have been used to incriminate infectious agents (mainly bacteria) as the cause of coral diseases without relating the agent to specific changes in cell and tissue pathology. Of 19 papers that declared an infectious agent as a cause of disease in corals, only one (5%) used microscopic pathology, and none fulfilled all of the criteria required to satisfy Koch’s postulates as applied to animal diseases currently. Vertebrate diseases of skin and mucosal surfaces present challenges similar to corals when trying to identify a pathogen from a vast array of environmental microbes, and diagnostic approaches regularly used in these cases might provide a model for investigating coral diseases. We hope this review will encourage specialists of disease in domestic animals, wildlife, fish, shellfish, and humans to contribute to the emerging field of coral disease.

EcoHealth↗
USGS2014

Evaluation of monkeypox virus infection of prairie dogs (Cynomys ludovicianus) using in vivo bioluminescent imaging

Monkeypox (MPX) is a re-emerging zoonotic disease that is endemic in Central and West Africa, where it can cause a smallpox-like disease in humans. Despite many epidemiologic and field investigations of MPX, no definitive reservoir species has been identified. Using recombinant viruses expressing the firefly luciferase (luc) gene, we previously demonstrated the suitability of in vivo bioluminescent imaging (BLI) to study the pathogenesis of MPX in animal models. Here, we evaluated BLI as a novel approach for tracking MPX virus infection in black-tailed prairie dogs (Cynomys ludovicianus). Prairie dogs were affected during a multistate outbreak of MPX in the US in 2003 and have since been used as an animal model of this disease. Our BLI results were compared with PCR and virus isolation from tissues collected postmortem. Virus was easily detected and quantified in skin and superficial tissues by BLI before and during clinical phases, as well as in subclinical secondary cases, but was not reliably detected in deep tissues such as the lung. Although there are limitations to viral detection in larger wild rodent species, BLI can enhance the use of prairie dogs as an animal model of MPX and can be used for the study of infection, disease progression, and transmission in potential wild rodent reservoirs.

South Dakota↗
USGS2014

Nonlethal screening of bat-wing skin with the use of ultraviolet fluorescence to detect lesions indicative of white-nose syndrome

Definitive diagnosis of the bat disease white-nose syndrome (WNS) requires histologic analysis to identify the cutaneous erosions caused by the fungal pathogen Pseudogymnoascus [formerly Geomyces] destructans (Pd). Gross visual inspection does not distinguish bats with or without WNS, and no nonlethal, on-site, preliminary screening methods are available for WNS in bats. We demonstrate that long-wave ultraviolet (UV) light (wavelength 368–385 nm) elicits a distinct orange–yellow fluorescence in bat-wing membranes (skin) that corresponds directly with the fungal cupping erosions in histologic sections of skin that are the current gold standard for diagnosis of WNS. Between March 2009 and April 2012, wing membranes from 168 North American bat carcasses submitted to the U.S. Geological Survey National Wildlife Health Center were examined with the use of both UV light and histology. Comparison of these techniques showed that 98.8% of the bats with foci of orange–yellow wing fluorescence (n = 80) were WNS-positive based on histologic diagnosis; bat wings that did not fluoresce under UV light (n = 88) were all histologically negative for WNS lesions. Punch biopsy samples as small as 3 mm taken from areas of wing with UV fluorescence were effective for identifying lesions diagnostic for WNS by histopathology. In a nonlethal biopsy-based study of 62 bats sampled (4-mm diameter) in hibernacula of the Czech Republic during 2012, 95.5% of fluorescent (n = 22) and 100% of nonfluorescent (n = 40) wing samples were confirmed by histopathology to be WNS positive and negative, respectively. This evidence supports use of long-wave UV light as a nonlethal and field-applicable method to screen bats for lesions indicative of WNS. Further, UV fluorescence can be used to guide targeted, nonlethal biopsy sampling for follow-up molecular testing, fungal culture analysis, and histologic confirmation of WNS.

Journal of Wildlife Diseases↗
USGS2014

Spatial and temporal patterns of avian paramyxovirus-1 outbreaks in Double-Crested Cormorants ( Phalacrocorax auritus ) in the USA

Morbidity and mortality events caused by avian paramyxovirus-1 (APMV-1) in Double-crested Cormorant (DCCO; Phalacrocorax auritus ) nesting colonies in the US and Canada have been sporadically documented in the literature. We describe APMV-1 associated outbreaks in DCCO in the US from the first reported occurrence in 1992 through 2012. The frequency of APMV-1 outbreaks has increased in the US over the last decade, but the majority of events have continued to occur in DCCO colonies in the Midwestern states. Although morbidity and mortality in conesting species has been frequently reported during DCCO APMV-1 outbreaks, our results suggest that isolation of APMV-1 is uncommon in species other than DCCO during APMV-1 outbreaks and that the cause of mortality in other species is associated with other pathogens. Populations of DCCO do not appear to have been significantly affected by this disease; however, because at least 65% of the APMV-1 outbreaks in DCCO in the US have involved APMV-1 strains classified as virulent to poultry (virulent Newcastle disease virus), its persistence and increased occurrence in DCCO warrants continued research and surveillance.

Journal of Wildlife Diseases↗
USGS2014

The fungus Trichophyton redellii sp. nov. causes skin infections that resemble white-nose syndrome of hibernating bats

Before the discovery of white-nose syndrome (WNS), a fungal disease caused by Pseudogymnoascus destructans , there were no reports of fungal skin infections in bats during hibernation. In 2011, bats with grossly visible fungal skin infections similar in appearance to WNS were reported from multiple sites in Wisconsin, USA, a state outside the known range of P. destructans and WNS at that time. Tape impressions or swab samples were collected from affected areas of skin from bats with these fungal infections in 2012 and analyzed by microscopy, culture, or direct DNA amplification and sequencing of the fungal internal transcribed spacer region (ITS). A psychrophilic species of Trichophyton was isolated in culture, detected by direct DNA amplification and sequencing, and observed on tape impressions. Deoxyribonucleic acid indicative of the same fungus was also detected on three of five bat carcasses collected in 2011 and 2012 from Wisconsin, Indiana, and Texas, USA. Superficial fungal skin infections caused by Trichophyton sp. were observed in histopathology for all three bats. Sequencing of the ITS of Trichophyton sp., along with its inability to grow at 25 C, indicated that it represented a previously unknown species, described herein as Trichophyton redellii sp. nov. Genetic diversity present within T. redellii suggests it is native to North America but that it had been overlooked before enhanced efforts to study fungi associated with bats in response to the emergence of WNS.

Journal of Wildlife Diseases↗
USGS2013

White-nose syndrome in bats: Illuminating the darkness

Happy ten-year anniversary to BMC Biology! We can attest to the effectiveness of the journal in reaching a great diversity of scientists based on reader responses to our commentary [1] about bat white-nose syndrome (WNS) two years ago. WNS is still on course to rank among the most destructive wildlife diseases to emerge in recent history, and it has continued to have unprecedented effects on populations of hibernating bats in eastern North America. At the time of our last writing in November 2010, the cold-adapted fungus then presumed to cause WNS ( Geomyces destructans ) had spread about 1,300 km from an index site in New York (Figure 1). In those early years of the epizootic, WNS caused a staggering wave of mass mortality among all six species of hibernating bats that occur in north-eastern North America. Since November 2010, WNS has spread into eight additional US states and two more Canadian provinces (Figure 1), and has continued to cause mortality in those six species most affected during the early years of the epizootic. Although part of a mostly tragic story has continued to unfold as new areas are affected, anecdotal signs are emerging that all may not be lost when it comes to hibernating bats and WNS. Amid the continued large-scale population declines of certain species, we have yet to see mass mortality in some of the more westerly areas where the fungus was detected two winters ago (Figure 1). Also, recently disease without obvious mortality was diagnosed in gray bats ( Myotis grisescens ) - an endangered species thought by many two years ago to be at high risk of extinction from WNS. Clearly, large gaps in our understanding of WNS remain, but some have been filled since we last communicated with readers of BMC Biology.

BMC Biology↗
USGS2013

A review of episodes of zinc phosphide toxicosis in wild geese (Branta spp.) in Oregon (2004−2011)

Epizootic mortality in several geese species, including cackling geese (Branta hutchinsii) and Canada geese (Branta canadensis), has been recognized in the Willamette Valley of Oregon for over a decade. Birds are generally found dead on a body of water or are occasionally observed displaying neurologic clinical signs such as an inability to raise or control the head prior to death. Investigation of these epizootic mortality events has revealed the etiology to be accidental poisoning with the rodenticide zinc phosphide (Zn 3 P 2 ). Gross and histologic changes are restricted to acute pulmonary congestion and edema, sometimes accompanied by distension of the upper alimentary tract by fresh grass. Geese are unusually susceptible to this pesticide; when combined with an epidemiologic confluence of depredation of specific agricultural crops by rodents and seasonal avian migration pathways, epizootic toxicosis may occur. Diagnosis requires a high index of suspicion, appropriate sample collection and handling, plus specific test calibration for this toxicant. Interagency cooperation, education of farmers regarding pesticide use, and enforcement of regulations has been successful in greatly decreasing these mortality events since 2009.

Oregon↗
USGS2013

Evidence of songbird intoxication from Rozol application at a black-tailed prairie dog colony

Concerns about avian poisonings from anticoagulant rodenticides have traditionally focused on secondary poisoning of raptors exposed by feeding on contaminated mammalian prey. However, ground foraging songbirds can be directly poisoned from operational applications of the anticoagulant rodenticide Rozol® (0.005% chlorophacinone, active ingredient) applied as a grain bait, at black-tailed prairie dog Cynomys ludovicianus colonies. A dead western meadowlark Sturnella neglecta recovered from the study prairie dog colony displayed hemorrhaging in brain and pectoral muscle tissue, and it contained chlorophacinone residue concentrations of 0.59 and 0.49 µg/g (wet weight) in the liver and intestinal contents, respectively. Chlorophacinone residues from two Rozol-colored songbird droppings found at the study colony were 0.09 and 0.46 µg/g (wet weight). The timing of the meadowlark mortality and the occurrence of discolored droppings show that songbird exposure and poisoning can occur weeks after a Rozol application.

Colorado↗
USGS2012

Frequent arousal from hibernation linked to severity of infection and mortality in bats with white-nose syndrome

White-nose syndrome (WNS), an emerging infectious disease that has killed over 5.5 million hibernating bats, is named for the causative agent, a white fungus (Geomyces destructans (Gd)) that invades the skin of torpid bats. During hibernation, arousals to warm (euthermic) body temperatures are normal but deplete fat stores. Temperature-sensitive dataloggers were attached to the backs of 504 free-ranging little brown bats (Myotis lucifugus) in hibernacula located throughout the northeastern USA. Dataloggers were retrieved at the end of the hibernation season and complete profiles of skin temperature data were available from 83 bats, which were categorized as: (1) unaffected, (2) WNS-affected but alive at time of datalogger removal, or (3) WNS-affected but found dead at time of datalogger removal. Histological confirmation of WNS severity (as indexed by degree of fungal infection) as well as confirmation of presence/absence of DNA from Gd by PCR was determined for 26 animals. We demonstrated that WNS-affected bats aroused to euthermic body temperatures more frequently than unaffected bats, likely contributing to subsequent mortality. Within the subset of WNS-affected bats that were found dead at the time of datalogger removal, the number of arousal bouts since datalogger attachment significantly predicted date of death. Additionally, the severity of cutaneous Gd infection correlated with the number of arousal episodes from torpor during hibernation. Thus, increased frequency of arousal from torpor likely contributes to WNS-associated mortality, but the question of how Gd infection induces increased arousals remains unanswered.

Michigan, Pennsylvania, Vermont, West Virginia↗
USGS2012

Assessment of toxicity and potential risk of the anticoagulant rodenticide diphacinone using Eastern screech-owls (Megascops asio)

In the United States, new regulatory restrictions have been placed on the use of some second-generation anticoagulant rodenticides. This action may be offset by expanded use of first-generation compounds (e.g., diphacinone; DPN). Single-day acute oral exposure of adult Eastern screech-owls (Megascops asio) to DPN evoked overt signs of intoxication, coagulopathy, histopathological lesions (e.g., hemorrhage, hepatocellular vacuolation), and/ or lethality at doses as low as 130 mg/kg body weight, although there was no dose-response relation. However, this single-day exposure protocol does not mimic the multiple-day field exposures required to cause mortality in rodent pest species and non-target birds and mammals. In 7-day feeding trials, similar toxic effects were observed in owls fed diets containing 2.15, 9.55 or 22.6 ppm DPN, but at a small fraction (<5%) of the acute oral dose. In the dietary trial, the average lowest-observed-adverse-effect-level for prolonged clotting time was 1.68 mg DPN/kg owl/week (0.24 mg/kg owl/day; 0.049 mg/owl/day) and the lowest lethal dose was 5.75 mg DPN/kg owl/week (0.82 mg/kg owl/day). In this feeding trial, DPN concentration in liver ranged from 0.473 to 2.21 &mu;g/g wet weight, and was directly related to the daily and cumulative dose consumed by each owl. A probabilistic risk assessment indicated that daily exposure to as little as 3-5 g of liver from DPN-poisoned rodents for 7 days could result in prolonged clotting time in the endangered Hawaiian shorteared owl (Asio flammeus sandwichensis) and Hawaiian hawk (Buteo solitarius), and daily exposure to greater quantities (9-13 g of liver) could result in low-level mortality. These findings can assist natural resource managers in weighing the costs and benefits of anticoagulant rodenticide use in pest control and eradication programs.

Ecotoxicology↗
USGS2012

Nonsteroidal anti-inflammatory drugs in raptors

The use of analgesia has become standard, and appropriate, practice in avian medicine. As in mammals, pain control in avian patients is usually accomplished with opioids and nonsteroidal anti-inflammatory drugs (NSAIDs) used singly or in combination for a multimodal approach. Despite their usefulness, widespread use, and relative safety in clinical use, few controlled studies in birds have been conducted on efficacy, safety, and dosing. The guidelines for the use of NSAIDs in raptors and other birds have mainly been empirical. More recently, NSAIDs in free-living raptors have emerged as a major conservation issue with the discovery that diclofenac sodium was responsible for the population crash of three species of Gyps vultures in southern Asia. In this context, residues of veterinary NSAIDs in domestic animals are now considered environmental contaminants that can be significantly toxic to vultures and possibly other avian scavengers. Ironically, the disaster with Asian vultures has led to a considerable body of research on NSAIDs in raptors to the benefit of clinicians who now have scientific information available to help assess dosing, safety, toxicity, and pharmacokinetics of NSAIDs in their raptor patients.

Book chapter↗