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Carol U. Meteyer

Publications and source records attributed to Carol U. Meteyer.

41 records · Page 3Linked to original sources

Peracute sodium toxicity in free-ranging black-bellied whistling duck ducklings

From 23 to 25 July 2002, 98–103 newly hatched black-bellied whistling ducks ( Dendrocygna autumnalis ) were observed alive at an inland saline lake (La Sal Vieja) in Willacy County, Texas (USA). Seventy-one (71%) died after showing signs indicative of sodium toxicity within 5 hr of entering the water; some died within minutes. Six carcasses were sent to the United States Geological Survey, National Wildlife Health Center (Madison, Wisconsin, USA) for analysis, and brain sodium levels of all ducklings were above 2,000 parts per million wet weight. More black-bellied whistling duck ducklings are likely to have been affected, but they were not observed after hatching.

Texas

Field guide to malformations of frogs and toads: with radiographic interpretations

In 1995, students found numerous malformed frogs on a field trip to a Minnesota pond. Since that time, reports of malformed frogs have increased dramatically. Malformed frogs have now been reported in 44 states in 38 species of frogs, and 19 species of toads. Estimates as high as 60% of the newly metamorphosed frog populations have had malformations at some ponds (NARCAM, ’99). The wide geographic distribution of malformed frogs and the variety of malformations are a concern to resource managers, research scientists and public health officials. The potential for malformations to serve as a signal of ecosystem disruption, and the affect this potential disruption might have on other organisms that share those ecosystems, has not been resolved. Malformations represent an error that occurred early in development. The event that caused the developmental error is temporally distant from the malformation we see in the fully developed animal. Knowledge of normal developmental principles is necessary to design thoughtful investigations that will define the events involved in abnormal development in wild frog populations. Development begins at the time an egg is fertilized and progresses by chemical communication between cells and cell layers. This communication is programmed through gene expression. Malformations represent primary errors in development, errors in chemical communication or translation of genetic information. Deformations arise later in development and usually result from the influence of mechanical factors (such as amputation) that alter shape or anatomy of a structure that has developed normally. The occurrence and the type of malformations are influenced by the type of error or insult as well as the timing of the error (the developmental stage at which the error occurred). The appearance of the malformation can therefore provide clues that suggest when the error may have occurred. If the malformation is an incomplete organ, such as an incomplete limb, the factor or insult acted during a susceptible period prior to organ completion. Although defining the anatomy of the malformed metamorphosed frog can give us an idea of the approximate window during which the developmental insult was initiated, and might even suggest the type of insult that may have occurred, the morphology of the malformation does not define the cause. To define causes and mechanisms of frog malformations we need to use well designed investigations that are different from traditional tests used in acute toxicity or disease pathogenicity studies. When investigating malformations in metamorphosed frogs, we are looking at the affect of exposure to an agent that occurred early in tadpole development. Therefore investigations to determine causes of malformations need to look at agents that are present in the tadpoles or their environments at these early developmental times. Laboratory experiments need to expose embryos and tadpoles to suspect agents at appropriate developmental stages and look at acute results, such as toxicity and death, as well as following the developmental process to completion to determine the impact of the agent on the developing tadpole and the fully developed frog. This means holding animals past metamorphic climax to assure that the anatomy and physiology of the adult have developed normally. As we look at field collections of abnormal frogs, we need to keep in mind that these collections reflect survivors only. We are looking at malformations that were not fatal to tadpoles. We cannot assume that because we do not collect other malformations, they did not exist. More work needs to be done on the developing tadpole, in the field and in the laboratory, to better elucidate the range, frequency, character and causes of anuran malformations.

Biological Science Report

Diagnostic findings in the 1992 epornitic of neurotropic velogenic Newcastle disease in double-crested cormorants from the upper midwestern United States

Neurotropic velogenic Newcastle disease (NVND) occurred in juvenile double-crested cormorants, Phalacrocorax auritus , simultaneously in nesting colonies in Minnesota, North Dakota, South Dakota, and Nebraska and in Lakes Michigan, Superior, Huron, and Ontario during the summer of 1992. Mortality as high as 80%-90% was estimated in some of the nesting colonies. Clinical signs observed in 4- to -6 wk-old cormorants included torticollis, tremors, ataxia, curled toes, and paresis or weakness of legs, wings or both, which was sometimes unilateral. No significant mortality or unusual clinical signs were seen in adult cormorants. Necropsy of 88 cormorants yielded no consistent gross observations. Microscopic lesions in the brain and spinal cord were consistently present in all cormorants from which Newcastle disease virus (NDV) was isolated. Characteristic brain lesions provided rapid identification of new suspect sites of NVND. Lesions were also present in the heart, kidney, proventriculus, spleen, and pancreas but were less consistent or nonspecific. NDV was isolated at the National Wildlife Health Center from 27 of 93 cormorants tested. Virus was most frequently isolated from intestine or brain tissue of cormorants submitted within the first 4wk of the epornitic. Sera collected from cormorants with neurologic signs were consistently positive for NDV antibody.The NDV isolate from cormorants was characterized as NVND virus at the National Veterinary Services Laboratories Ames, Iowa. The NVND virus was also identified as the cause of neurologic disease in a North Dakota turkey flock during the summer of 1992. Although no virus was isolated from cormorants tested after the first month of submissions, brain and spinal cord lesions characteristic of NVND were observed in cormorants from affected sites for 2 mo, at which time nesting colonies dispersed and no more submissions were received. Risk to susceptible populations of both wild avian species and domestic poultry makes early recognition and confirmation of NVND in wild birds a priority.

Minnesota, Nebraska, North Dakota, South Dakota

Mortality of passerines adjacent to a North Carolina corn field treated with granular carbofuran

Red-winged blackbirds ( Agelaius phoeniceus ) were collected during an epizootic in southeastern North Carolina (USA). Activity of brain cholinesterase (ChE) was inhibited by 14 to 48% in three of five specimens, and returned to normal levels after incubation. Gastrointestinal tracts were analyzed for 30 anti-ChE agents. Carbofuran, the only compound detected, was present in all specimens at levels from 5.44 to 72.7 μg/g wet weight. Application of granular carbofuran in an adjacent corn field, results of necropsy examinations, and chemical analyses are consistent with a diagnosis of carbofuran poisoning in these specimens.

North Carolina

Lead poisoning of spectacled eiders (Somateria fischeri) and of a common eider (Somateria mollissima) in Alaska

Lead poisoning was diagnosed in four spectacled eiders ( Somateria fischeri ) and one common eider ( Somateria mollissima ) found dead or moribund at the Yukon Delta National Wildlife Refuge, Alaska (USA) in 1992, 1993, and 1994. Ingested lead shot was found in the lower esophagus of one spectacled eider and in the gizzard of the common eider. Lead concentrations in the livers of the spectacled eiders were 26 to 38 ppm wet weight, and 52 ppm wet weight in the liver of the common eider. A blood sample collected from one of the spectacled eiders before it was euthanized had a lead concentration of 8.5 ppm wet weight. This is the first known report of lead poisoning in the spectacled eider, recently listed as a threatened species by the U.S. Fish and Wildlife Service.

Alaska