Geology topics

Linda C. Glaser

Publications and source records attributed to Linda C. Glaser.

3 recordsLinked to original sources

USGS1999

Health evaluation of Columbian white-tailed deer on Julia Butler Hansen Refuge for the Columbian white-tailed deer

The Columbian white-tailed deer ( Odocoileus virginianus leucurus) was designated an endangered species in 1968. At that time the estimated population along the lower Columbia River of Washington and Oregon was 300 to 400 deer (Gavin, 1984). The Julia Butler Hansen Refuge for the Columbian White-tailed Deer was established in 1972 to protect Columbian white-tailed deer and associated habitat Currently, an estimated 600 deer are present in several separate populations. The total refuge population is estimated at 200 animals. Of those, the mainland population consists of approximately 60 animals while the largest refuge island (Tenasillahe.Island) supports about 120 animals. The remaining 420 deer are present on private lands near the refuge (AI Clark, pers. com.). Higher than expected deer mortality on Tenasillahe Island in the spring of 1996 prompted refuge personnel to request assistance from the National Wildlife Health Center (NWHC) for diagnostic evaluation to determine the cause of the mortalities. The mortality event occurred in the wake of extraordinary .flooding that reduced the availability and quality of forage on the island. It is estimated that 50% of the deer population on the refuge died during this time period. The basic finding of emaciation attributable to probable starvation raised concerns regarding the health status of the deer herd, available food resources, and current population levels. A health evaluation was conducted on free-ranging deer from the refuge in February, 1998. This evaluation was an analysis of physiologic parameters obtained from live deer in an attempt to determine the health of individual animals and, with adequate sampling, the health of the population. This study was conducted during February to examine individual animal health during the seasonal period when the deer are in their poorest physical condition. The late winter period prior to spring green-up is a time when the effects ofbreeding and winter stress are most evident (Venne and Ozoga, 1971). The objectives of this study were to: (1) gather baseline physiologic data on a subset of the population, (2) evaluate the data to determine the health of the animals sampled, (3) if possible, identify causes of poor health and, ( 4) provide refuge personnel with information that will aid them in managing the population.

Oregon, Washington↗

USGS1997

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↗

USGS1995

Wildlife mortality attributed to organophosphorus and carbamate pesticides

Organophosphorus (OP) and carbamate pesticides are used widely in agricultural and residential applications as insecticides, herbicides, fungicides, and rodenticides. This family of chemicals replaced the organochlorine pesticides banned for use in the United States in the 1970's. Unlike organochlorine pesticides, which are long-lived in the environment and cause biological damage when they accumulate in an organism's system over time, OP and carbamate pesticides are short-lived in the environment and fast-acting on their "target pest." Direct mortality of wildlife from organochlorine pesticides was uncommon (Hayes and Wayland 1975); however, mortality is the primary documented effect on wildlife from OP and carbamate pesticides (Grue et al. 1983). Organophosphorus and carbamate pesticide toxicity is not specific to a target "pest," and lethal effects are seen in nontarget organisms; birds appear to be the most sensitive class of animals affected by these pesticides. Organophosphorus and carbamate pesticides primarily affect the nervous system by inhibiting acetylcholinesterase (AChE) enzyme activity. This enzyme's main function in the nervous system is to break down the neurotransmitter acetylcholine. When AChE is altered by OP and carbamate pesticides, it cannot perform this breakdown function and acetylcholine accumulates. Acetylcholine accumulation increases nerve impulse transmission and leads to nerve exhaustion and, ultimately, failure of the nervous system. When the nervous system fails, muscles do not receive the electrical input they require to move. The respiratory muscles are the most critical muscle group affected, and respiratory paralysis is often the immediate cause of death.

Book chapter↗