Search Results
You are looking at 1 - 10 of 11 items for
- Author or Editor: Birgit Puschner x
- Refine by Access: All Content x
Abstract
Objective—To determine deployment logistics of New York Police Department (NYPD) working dogs that assisted in relief efforts at the World Trade Center (WTC) site following the September 11, 2001, terrorist attack; establish types and rates of related acute injuries and illnesses; identify environmental toxin exposures; and determine long-term (ie, 5-year) health effects of deployment.
Design—Prospective cohort study.
Animals—27 working dogs.
Procedures—Deployment logistics for the period from September 11, 2001, through May 30, 2002, were determined, and acute health disorders were identified by means of physical examination; a questionnaire; interviews with dog handlers; and toxicologic (blood and hair samples), clinicopathologic, microbiologic (nasal swab specimens submitted for Bacillus anthracis culture), and radiographic methods. Long-term health surveillance ended September 21, 2006.
Results—Dogs worked a total of 1,428 days (15,148 hours) at the site. Seventeen of the 27 (62.9%) dogs had health disorders during the first week. Specific conditions included fatigue (incidence rate [events/1,000 active deployment hours], 13.1), conjunctival irritation (13.1), respiratory tract problems (12.4), decreased appetite (10.8), dehydration (10), and cuts (9.3). Only minor hematologic and serum biochemical abnormalities were identified. Bacterial culture of nasal swab specimens did not yield B anthracis. Only mild and infrequent health conditions were identified during the 5-year follow-up period. None of the dogs were identified as having chronic respiratory tract disease. Six dogs died of various causes.
Conclusions and Clinical Relevance—Results suggested that acute injuries and illnesses were common among NYPD working dogs deployed to the WTC disaster site, but that longterm health complications were minimal.
Abstract
Objective—To determine concentrations of α-tocopherol in serum and CSF of healthy horses following administration of supplemental vitamin E in feed.
Animals—10 healthy adult horses.
Procedures—Horses were allocated to receive supplemental d-α-tocopherol (1,000 U/d [group A; n = 5] or 10,000 U/d [group B; 5]) in feed for 10 days. Blood samples were collected before (baseline), during, and at intervals for 10 days after discontinuation of vitamin E administration for assessment of serum α-tocopherol concentration. Cerebrospinal fluid samples were collected prior to and 24 hours after cessation of vitamin E administration. α-Tocopherol concentrations in serum and CSF samples were analyzed via high-performance liquid chromatography; changes in those values during the treatment period were compared between groups, and the relationship of serum and CSF α-tocopherol concentrations was evaluated.
Results—In both groups, serum α-tocopherol concentration increased significantly from baseline during vitamin E administration; values in group B were significantly greater than those in group A during and after treatment. At the end of vitamin E administration, CSF α-tocopherol concentration was not significantly greater than the baseline value in either group; however, the increase in CSF concentration was significant when the group data were combined and analyzed. Serum and CSF α-tocopherol concentrations were significantly correlated at baseline for all horses, but were not strongly correlated after 10 days of vitamin E administration.
Conclusions and Clinical Relevance—In healthy horses, daily oral administration of supplemental vitamin E in feed resulted in increases in serum and CSF α-tocopherol concentrations.
Abstract
Objective—To quantitate the effects of desflurane and mode of ventilation on cardiovascular and respiratory functions and identify changes in selected clinicopathologic variables and serum fluoride values associated with desflurane anesthesia in horses.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized on 2 occasions: first, to determine the minimum alveolar concentration (MAC) of desflurane in O2 and second, to characterize cardiopulmonary and clinicopathologic responses to 1×, 1.5×, and 1.75× desflurane MAC during both controlled and spontaneous ventilation.
Results—Mean ± SEM MAC of desflurane in horses was 8.06 ± 0.41%; inhalation of desflurane did not appear to cause airway irritation. During spontaneous ventilation, mean PaCO2 was 69 mm Hg. Arterial blood pressure, stroke volume, and cardiac output decreased as the dose of desflurane increased. Conditions of intermittent positive pressure ventilation and eucapnia resulted in further cardiovascular depression. Horses recovered quickly from anesthesia with little transient or no clinicopathologic evidence of adverse effects. Serum fluoride concentration before and after administration of desflurane was below the limit of detection of 0.05 ppm (2.63µM/L).
Conclusions and Clinical Relevance—Results indicate that desflurane, like other inhalation anesthetics, causes profound hypoventilation in horses. The magnitude of cardiovascular depression is related to dose and mode of ventilation; cardiovascular depression is less severe at doses of 1× to 1.5× MAC, compared with known effects of other inhalation anesthetics under similar conditions. Desflurane is not metabolized to an important degree and does not appear to prominently influence renal function or hepatic cellular integrity or function. ( Am J Vet Res 2005;66:669–677)
Abstract
Case Description—A closed herd of 400 mixed-breed dairy goats was examined because of a decrease in milk production and increase in mortality rate. Nine animals had died within a 1-month period.
Clinical Findings—Clinical signs were evident only in lactating goats and included anorexia and recumbency. In the most severely affected goats, signs progressed to neurologic abnormalities and death. Serum aspartate aminotransferase activity, γ-glutamyltransferase activity, and total bilirubin concentration were high in clinically affected does, but no evidence of hemolysis was found. A diagnosis of copper toxicosis was made on the basis of high liver and kidney copper concentrations and histologic evidence of hepatic necrosis. Goats were found to have been fed a mineral mix containing 3,050 ppm copper for 9 months prior to the onset of copper toxicosis. Overall, there was no consistent relationship between serum hepatic enzyme activities, serum copper concentration, and liver copper concentration.
Treatment and Outcome—Clinically affected goats were treated with penicillamine, ammonium molybdate, sodium thiosulfate, and vitamin E. Penicillamine increased urine copper excretion in treated does versus untreated control animals. An increased incidence of infectious disease was identified in the herd 9 months later. Liver vitamin E concentration was low in 10 of the 12 goats that underwent necropsy.
Clinical Relevance—Findings suggested that penicillamine may be an effective treatment for goats with copper toxicosis. Production losses months after the diagnosis was made suggested that the intoxication had a prolonged animal welfare and economic impacts.
Abstract
Objective—To characterize the clinical and clinicopathologic effects and evaluate outcome associated with oleander toxicosis in New World camelids.
Design—Retrospective case series.
Animals—11 llamas and 1 alpaca.
Procedures—Medical records from a veterinary medical teaching hospital from January 1, 1995, to December 31, 2006, were reviewed. Records of all New World camelids that had detectable amounts of oleandrin in samples of serum, urine, or gastrointestinal fluid were included in the study. Descriptive statistics were used to evaluate the history, physical examination findings, clinicopathologic data, and outcome of affected camelids.
Results—11 llamas and 1 alpaca met the inclusion criteria of the study. Either oleander plants were present where the camelids resided (n = 7) or oleander plant material was identified in the hay fed to the camelids (5). One llama was dead on arrival at the hospital, and another was euthanized upon admission because of financial concerns. Of the 10 treated camelids, 9 had evidence of acute renal failure, 7 had gastrointestinal signs, and 4 had cardiac dysrhythmias on initial evaluation. The overall mortality rate was 25%, but the mortality rate for the 10 camelids that were medically treated was 10%.
Conclusions and Clinical Relevance—In New World camelids, oleander intoxication was associated with a triad of clinical effects (ie, renal, gastrointestinal, and cardiovascular dysfunction). Oleander intoxication often represented a herd problem but carried a fair to good prognosis if treated promptly. Oleander toxicosis should be considered a differential diagnosis in sick camelids.
Abstract
Case Description—2 dogs (dogs 1 and 2) were examined for sudden onset of blindness. Both dogs had mild obtundation and mydriasis in both eyes. It was thought that dog 1 may have ingested ivermectin; dog 2 had been treated with ivermectin for demodectic mange.
Clinical Findings—On initial examination, both dogs had mydriasis and decreased pupillary light reflexes in both eyes. Dog 1 had an absent menace response bilaterally. Fundic examination of both eyes in both dogs revealed regions of multifocal retinal edema and folds with low-lying retinal separation. The electroretinogram was extinguished in dog 1 and attenuated in dog 2. Ivermectin was detected in serum samples from both dogs.
Treatment and Outcome—Both dogs made a complete clinical recovery following cessation of exposure to ivermectin; electroretinographic findings improved, and retinal edema resolved with some residual chorioretinal scarring.
Clinical Relevance—To our knowledge, this is the first report of resolution of retinal edema and electroretinographic changes associated with ivermectin toxicosis in dogs. In dogs that develop blindness suddenly, fundic examination, electroretinography, and assessment of serum ivermectin concentration are diagnostically useful, even if exposure to ivermectin is unknown.
Abstract
Objective—To quantitate effects of dose of sevoflurane and mode of ventilation on cardiovascular and respiratory function in horses and identify changes in serum biochemical values associated with sevoflurane anesthesia.
Animals—6 healthy adult horses.
Procedure—Horses were anesthetized twice: first, to determine the minimum alveolar concentration (MAC) of sevoflurane and second, to characterize cardiopulmonary and serum biochemical responses of horses to 1.0, 1.5, and 1.75 MAC multiples of sevoflurane during controlled and spontaneous ventilation.
Results—Mean (± SEM) MAC of sevoflurane was 2.84 ± 0.16%. Cardiovascular performance during anesthesia decreased as sevoflurane dose increased; the magnitude of cardiovascular depression was more severe during mechanical ventilation, compared with spontaneous ventilation. Serum inorganic fluoride concentration increased to a peak of 50.8 ± 7.1 µmol/L at the end of anesthesia. Serum creatinine concentration and sorbitol dehydrogenase activity reached their greatest values (2.0 ± 0.8 mg/dL and 10.2 ± 1.8 U/L, respectively) at 1 hour after anesthesia and then returned to baseline by 1 day after anesthesia. Serum creatine kinase, aspartate aminotransferase, and alkaline phosphatase activities reached peak values by the first (ie, creatine kinase) or second (ie, aspartate aminotransferase and alkaline phosphatase) day after anesthesia.
Conclusions and Clinical Relevance—Sevoflurane causes dose-related cardiopulmonary depression, and mode of ventilation further impacts the magnitude of this depression. Except for serum inorganic fluoride concentration, quantitative alterations in serum biochemical indices of liver- and muscle-cell disruption and kidney function were considered clinically unremarkable and similar to results from comparable studies of other inhalation anesthetics. (Am J Vet Res 2005;66:606–614)
Abstract
Objective—To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm.
Design—Prospective case series.
Animals—148 horses.
Procedures—Neurologic, pathological, and toxicological evaluations were completed in selected neurologically affected horses over a 2-year period. Descriptive statistical analysis was performed.
Results—87 QHs and 1 QH-crossbred horse were affected. Most (50/88 [56.8%]) affected horses were 1 to 2 years old (median age, 2 years [range, 2 months to 34 years]). Neurologic deficits included obtundation (53/88 [60%] horses), decreased to absent menace response (33/88 [37.5%]), proprioceptive positioning deficits, wide-based stance, ataxia, and dysmetria (88/88 [100%]). Most (78/88 [88.6%]) horses had mild ataxia, but some (10/88 [11.4%]) had moderate to severe ataxia. Low serum concentrations of vitamin E (≤ 2 mg/L) were detected in 3 index case horses and 16 of 17 randomly selected horses (13/14 affected and 3/3 unaffected) during study year 1. Dietary vitamin E supplementation did not improve neurologic deficits in affected horses; vitamin E administration in pregnant mares appeared to decrease but not prevent disease development among offspring born the following year. Lesions detected at necropsy included bilaterally symmetric neuroaxonal degeneration with axonal spheroids in the nucleus gracilis, nucleus cuneatus medialis, nucleus cuneatus lateralis, and nucleus thoracicus (5/5 horses).
Conclusions and Clinical Relevance—Neuroaxonal dystrophy should be considered in evaluation of young horses with ataxia and proprioceptive positioning deficits. Vitamin E deficiency may contribute to disease severity.
