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.
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)
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.
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
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
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)
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.
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.
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.
Objective—To determine thiamine-dependent enzyme activities in various tissue samples of Pacific harbor seals (Phoca vitulina) and thiaminase activities in dietary fish.
Animals—11 Pacific harbor seals with thiamine deficiency and 5 control seals.
Procedures—Seals underwent evaluation to rule out various diseases and exposure to toxins. For seals that died, measurement of thiamine-dependent enzymes in liver and brain samples and determination of mitochondrial DNA (mtDNA) copy number in liver, brain, and muscle samples were performed. Thiaminase activity in dietary fish was determined.
Results—8 seals with thiamine deficiency died. Affected seals typically had acute neurologic signs with few nonspecific findings detected by means of clinicopathologic tests and histologic examination of tissue samples. Thiamine-dependent enzyme activities in liver samples of affected seals were significantly lower than those in control liver samples. The primary activation ratios and latencies for enzymes indicated that brain tissue was more affected by thiamine deficiency than liver tissue. Activities of pyruvate dehydrogenase were more affected by thiamine deficiency than those of transketolase and ketoglutarate dehydrogenase. For control seals, the mtDNA copy number in muscle samples was significantly lower than that for affected seals; conversely, the copy number in control liver samples was significantly greater than that of affected seals. Thiaminase activity was substantially higher in smelt than it was in other types of dietary fish.
Conclusions and Clinical Relevance—Results of analyses in this study confirmed a diagnosis of thiamine deficiency for affected seals resulting from high thiaminase activity in dietary fish, inadequate vitamin administration, and increased thiamine demand caused by pregnancy and lactation.
Objective—To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm.
Design—Prospective case series.
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.