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Lead intoxication is rarely diagnosed in horses and can present a major challenge to the equine practitioner because of the variety of clinical signs. Horses with lead poisoning can develop gastrointestinal disturbances, neurological abnormalities, haematological changes, or nonspecific signs of weight loss, weakness and rough hair coat, which makes early diagnosis difficult. Fortunately, lead analysis of whole blood is routinely available and can confirm intoxication. Because of the well‐described lead‐induced peripheral neuropathies in horses, a thorough neurological examination is essential in the investigation of a suspect case. Once diagnosed, the source of lead has to be identified and further exposure prevented. Intoxication can be treated by administering chelating drugs and providing symptomatic and supportive care.  相似文献   

3.
Two experiments were conducted to study the metabolism and tissue accumulation and depletion of dietary Pb in sheep. In Exp. 1, a feeding trial, 33 wethers, 56 kg initially, were assigned randomly to two dietary treatments: .25% Ca plus 1,000 ppm Pb or .50% Ca plus 1,000 ppm Pb. Supplemental Ca and Pb were supplied as reagent grade calcium carbonate or reagent grade lead acetate. The experiment was divided into two phases of 75 and 180 d; during the first phase, diets contained 1,000 ppm supplemental Pb and during the second phase, diets contained 3 ppm Pb. Calcium level remained constant within treatments throughout both phases. Sheep were slaughtered at various intervals during both phases and tissue samples taken. Lead increased in all tissues during the accumulation period and decreased during the depletion period; however, kidney was the only tissue in which Pb concentration declined to control values by 180 d. Dietary Ca reduced (P less than .05) the concentration of Pb deposited in liver, but not in other tissues. Interactions of dietary Ca and Pb on tissue concentration of various minerals occurred. In Exp. 2, a balance trial, 27 wethers, 53 kg initially, were allotted randomly to four treatments in a 2 X 2 factorial arrangement. Diets contained either 0 or 1,000 ppm supplemental Pb as reagent grade lead acetate and .25 or .50% total Ca with supplemental Ca from calcium carbonate. Increasing dietary Pb increased (P less than .05) percentage of Pb retained and increased (P less than .01) whole blood Pb concentration (1.0 vs 1.42 micrograms/ml).  相似文献   

4.
Laboratory and field experiments involving more than 100,000 birds were performed to assess the effect of simultaneous in-feed medication of chickens with salinomycin and tiamulin at various concentrations. In an artificial infection study with Mycoplasma gallisepticum, low levels of tiamulin (10-40 ppm) did not induce signs of ionophore intoxication with salinomycin at 60 ppm in the feed, whereas levels of 50 ppm caused early signs with a mild growth depression. A level of 20 ppm gave a maximum average improvement in growth rate of 12.5%. There was a dose-related response in mycoplasma lesion inhibition, with 50 ppm reducing lesions by 75%. In the two field trials, chickens suffering from mycoplasmosis complicated with infectious bronchitis and receiving 60 ppm salinomycin in the feed showed marked improvements in mortality rates, lesion scores, and feed-conversion efficiency when tiamulin was added at 20 ppm and 30 ppm in the feed. There were no signs of incompatibility between the two antibiotics at these levels.  相似文献   

5.
Observations  A case of a pony with severe cyanide intoxication as a result of cherry ingestion is presented. General anaesthesia was performed for colic surgery. Severe metabolic lactate acidosis in combination with a high arterial oxygen partial pressure and clinically good peripheral perfusion parameters were the remarkable signs during anaesthesia. Severe hypothermia was obvious during recovery. Ten hours post-surgery the pony was euthanized as a result of neurological signs. The diagnosis of cyanide intoxication was made post-mortem.
Conclusion  Cherry ingestion can lead to lethal cyanide intoxication in horses indicated by severe nonhypoxic lactic acidosis during anaesthesia.  相似文献   

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Lead acetate was fed to 4 groups of 2 horses each to study chronic lead intoxication. A 5th group of 3 horses was maintained as controls. The leas was fed in capsules, with the minimum dosage of 6.25 mg/kg/day of lead as lead acetate (group I). The dose was increased from group I through group IV in an approximate geometric series, with each group being given about 125% of the dose given the previous group. These doses were given for 105 days, a period designated as phase 1. Since clinical signs were not observed after 105 days, the doses were increased and fed for an additional 190 days (days 106 to 295). This period was designated phase 2. The smallest daily dose in phase 2 was set at about 125% of the largest daily dose in phase 1. The doses in each group was increased by about 125% of that of the previous group, as was done in phase 1. Seven horses died or were euthanatized after 18 to 190 days of phase 2 (123 to 295 days after the 1st dose). One horse in group I did not develop any clinical signs of intoxication. Dose-related responses were unnoticed with doses larger than 15.3 mg/kg/day. All horses given lead had increased blood lead and serum iron concentrations. During phase 2, the hematocrit (erythrocyte volume) and hemoglobin contents were depressed. The lead concentration in kidney, liver, spleen, pancreas, brain, bone, and heart was increased in the treated horses. The dose level required to produce lead intoxication was greater than that reported for cattle and that estimated in epizootiologic studies of horses.  相似文献   

8.
Three experiments were conducted to study the clinical and pathological findings associated with poisoning in cattle due to ingestion of young oak leaves (OL) and the main factors responsible for toxicosis. In Experiment 1, six 1.4 year-old bulls were fed up to 5 kg of young OL per animal per day and showed no signs of toxicity, apart from a slight proteinuria. In Experiment 2, another six 1.4 year-old bulls were first subjected to severe feed restriction for eight days and then fed a higher amount of OL (approx. 10 kg) daily. A marked increase of serum creatinine and blood urea (BUN) was detected in urine as well as clinical signs consistent with renal failure. At necropsy, animals showed gastrointestinal ulcers and kidney tubular necrosis. Since these results suggested a crucial role of the feed restricting period, a third experiment was conducted administering the same amount of young OL as in Experiment 1, but adding the severe feed restricting period as in Experiment 2. There was a wide variation in clinical signs, with one bull showing clinical signs and lesions, another recovering after showing mild clinical signs and high levels of creatinine and BUN, and the third appearing clinically normal. The relevance of restriction access to food in the development of OL toxicosis appears to be critical because the intoxication was only elicited when the OL administration was preceded by a severe feed restricting period.  相似文献   

9.
Anamnesis and clinical signs of horses form five different stables after ingestion of ionophores are reported and techniques of feed examination are described. Within a few hours or days after feeding of new types or batches of concentrates horses fell ill. They showed colic-like symptoms with intense sweating and ataxia. Most of the sick animals died within a short time span. Samples of the concentrates were analysed and different types and amounts of ionophores were detected. In four cases contamination by monensin in concentrations of less than 5 mg to 679 mg/kg feed were found. One feed sample contained monensin (8.8 mg/kg feed) as well as salinomycin (67.3 mg/kg feed). In one case lasalocid (7.9 mg/kg feed) was present. One horse from the stable where animals had obtained concentrates containing monensin (679 mg/kg feed) was necropsied. Typical signs of monensin intoxication with severe myocardial degeneration were found. Veterinarians should be alert to this rare but severe intoxication of horses.  相似文献   

10.
Adult female mink were fed rations containing 1.1, 1.8, 4.8, 8.3 and 15.0 ppm mercury as methyl mercury chloride over a 93 day period. Histopathological evidence of injury was present in all groups. Mink fed rations containing 1.8 to 15.0 ppm mercury developed clinical intoxication within the experimental period. The rapidity of onset of clinical intoxication was directly related to the mercury content of the ration. Mercury concentration in tissue of mink which died were similar, despite differences in mercury content of the diets and time of death. The average mercury concentration in the brain of mink which died was 11.9 ppm. The lesions of methyl mercury poisoning are described and criteria for diagnosis are discussed.  相似文献   

11.
Objective: To describe the clinical consequences following ingestion by a dog of a moxidectin‐containing equine deworming product. Few reports exist concerning the treatment and outcome of severe moxidectin toxicity. Treatment, known factors influencing intoxication, and prognosis are reviewed. Case summary: A 10‐month‐old female Border Collie ingested an unknown quantity of a moxidectin‐containing equine deworming product several hours before presentation. Severe neurological signs subsequently developed and included: ataxia, seizures, coma, and respiratory failure. The dog was treated with supportive care including intravenous fluids, activated charcoal, and positive pressure ventilation. Normal spontaneous respiration returned in 34 hours and the patient was discharged 58 hours after ingestion. Full recovery occurred within 1 week of intoxication. New information provided: This report describes moxidectin intoxication and associated respiratory failure in a dog that required mechanical ventilation. The dog's recovery was rapid. Despite severity of signs, the prognosis for patients with moxidectin intoxication is good with appropriate supportive care.  相似文献   

12.
Lead poisoning was diagnosed in three cattle along with increased mercury levels in the liver and kidney tissues of two of these animals. The clinical signs were different in each case and included salivation, anorexia, delayed menace response, delayed withdrawal reflex, head pressing, localized muscle fasciculation, reduced tongue tone, ataxia, rumen atony and seizures. Blood lead concentration was increased in all three cases to 0.76, 0.37 and 0.454ppm. Post mortem changes characteristic of lead poisoning were only recognized in one case and included cerebro-cortical oedema, cortical neuronal necrosis and endothelial proliferation, especially at the tips of the cerebral gyri. The animals were poisoned by ingestion of lead-contaminated ash residues from a bonfire. The abnormal levels of mercury in the liver and kidney tissues of two animals may also be at least partly attributable to the intake of the metal in the ash residues. The levels of mercury in the three samples from the ash residue were relatively low (1.31, 0.7 and 2.1ppm).  相似文献   

13.
Calves were treated with different doses of lead acetate to investigate the influence of chronic subclinical lead intoxication on the immune system. A seven months old heifer fell ill showing typical signs of acute lead intoxication. This animal had been fed 0.316 mg lead for three months and 5 mg Pb/kg body weight/day for 17 days afterwards. Following symptoms were observed: Derangement of the central nervous system, paresis of the left body side, motor paralysis of the chewing muscles and disturbances of swallowing activity. Furthermore tooth grinding and attempts to push against, or climb walls were seen. After a single dose (2g) Ca-EDTA the heifer recovered progressively in 18 days.  相似文献   

14.
OBJECTIVE: To determine history, clinical and electrocardiographic abnormalities, treatment, and outcome of dogs exposed to toxins produced by the Bufo marinus toad. DESIGN: Retrospective study. ANIMALS: 94 dogs. PROCEDURE: Medical records of dogs examined between July 1997 and July 1998 for which a diagnosis of toad intoxication had been made on the basis of history and physical examination findings were reviewed. RESULTS: Most (66) dogs were treated during the spring and summer. For 54 dogs, exposure to toads had been witnessed. For the remaining 40, toad intoxication was diagnosed on the basis of history and clinical signs. The most common clinical signs were neurologic abnormalities, hyperemic mucous membranes, ptyalism, recumbency or collapse, tachypnea, and vomiting. The oral cavity was lavaged with tap water in all dogs. Fifty-two dogs were hospitalized for treatment. Body weight of dogs hospitalized > 2 hours was significantly less than that of dogs treated as outpatients. The most common electrocardiographic findings were sinus arrhythmia, sinus tachycardia, and normal sinus rhythm. Eighty-nine dogs recovered fully, 4 died, and 1 was euthanatized. CONCLUSIONS AND CLINICAL RELEVANCE: In areas in which B marinus toads are endemic, toad intoxication should be considered in the differential diagnosis for dogs with an acute onset of neurologic abnormalities, hyperemic mucous membranes, and ptyalism, especially during the spring and summer months. The prognosis is good for dogs with toad intoxication that receive appropriate treatment.  相似文献   

15.
The efficacy of meso-dimercaptosuccinic acid (DMSA) (succimer) in treating avian lead intoxication was studied in a retrospective, nonrandomized, longitudinal study. Nineteen birds with moderate to high blood lead concentration and neurologic signs compatible with lead toxicity were treated with DMSA (30 mg/kg p.o., b.i.d.; n = 15) for a minimum of 7 days. In cases with severe neurologic signs, DMSA was supplemented with a single dose of edetate calcium disodium (<50.0 mg/kg of body weight i.m.; n = 4). Blood lead concentrations were measured two or more times (before and after treatment). Median blood lead concentration decreased (87%), neurologic signs were resolved, and there were no apparent adverse secondary effects.  相似文献   

16.
Spontaneous intoxication in 34 horses after ingesting freshly harvested maize that was to be used for ensiling and heavily contaminated with young Datura stramonium plants, is described. The clinical status of all horses was monitored for 7 days, and included body (rectal) temperature, respiratory and heart rates, colour and moistness of visible mucosae, changes in pupil size, appetite, thirst, general behaviour, locomotion, sensory perceptions, urination and defaecation. The intoxication was accompanied by altered clinical status, namely mild hyperthermia, tachycardia, polypnoea, dyspnoea and shallow breathing, mydriasis, dry oral, rectal, vaginal and nasal mucosae, acute gastric dilatation and severe intestinal gas accumulation, anorexia to complete refusal of feed, decreased or absent thirst, absence of defaecation and urination. As a result of the treatment, the clinical parameters normalised between days 2 and 5. Necropsies and pathological studies were performed on two horses that died, revealing toxic liver dystrophy, cardiac lesions and substantial dystrophic and necrotic processes in the kidneys. The observed clinical signs, the pathomorphological changes and the applied therapy could be used in the diagnosis, differential diagnosis, prognosis and treatment of Jimson weed intoxication.  相似文献   

17.
BACKGROUND: Lead is a persistent contaminant in the environment, and waterfowl are susceptible to lead toxicity from ingestion of lead pellets and fishing weights. Lead affects numerous physiologic processes through inhibition of enzyme activity and protein function, but its effects on commonly assessed avian blood values are incompletely understood. OBJECTIVES: Our aim was to evaluate hematologic and biochemical changes associated with blood lead concentrations in trumpeter swans and Canada geese. METHODS: Data for CBCs, plasma biochemical profiles (total protein, albumin, glucose, cholesterol, total bilirubin, calcium, phosphorus, gamma-glutamyltransferase [GGT], aspartate aminotransferase, lactate dehydrogenase, glutamate dehydrogenase, creatine kinase, amylase, and lipase), and whole blood lead concentrations were retrospectively analyzed for 69 trumpeter swans and 52 Canada geese. Laboratory data obtained prospectively from an additional 20 trumpeter swans also were included. RBC morphology was semiquantitated in blood smears from 70 of the birds. Data were analyzed initially by ANOVA and covariance. A statistical model then was constructed to determine the relationship between each parameter and lead concentration. RESULTS: In both avian species, PCV, hemoglobin concentration, and MCHC decreased significantly (P < .05) with increasing blood lead concentration. Uric acid concentration and GGT activity were increased in trumpeter swans and phosphorus concentration was decreased in Canada geese in association with high blood lead concentration (P < .05). CONCLUSIONS: Lead toxicosis induced significant changes in the values of commonly measured hematologic parameters in waterfowl. These changes may be useful indicators of severe lead intoxication during routine laboratory assessment. Changes in clinical chemistry values, although statistically significant, were too inconsistent to serve as indicators of lead toxicosis.  相似文献   

18.
Results of experimental studiesindicate that horses are much more sensitive to monensin toxicity than cattle. Single dose studies by gavage with mycelial monensin resulted in an estimated LD50 of 1.38 mg/kg of body weight. Subacute feeding studies indicate that horses will tolerate the highest use level for cattle of 33 ppm without any evidence of toxicity. Evidence of intoxication was apparent with the highest use level for chickens of 121 ppm.In pasture supplement studies, horses ate supplement containing high levels of nonensin upon initial exposure which resulted in toxicity and/or death. Following initial exposure to sublethal levels, consumption of monensin containing supplements was negligible.The clinical signs of toxicity includedpartial to complete anorexia, colicky pain, sweating and tachycardia, uneasiness, polyuria, progressive ataxia, recumbency with frequent attempts to rise and thrashing of the limbs followed by death. Examination at necropsy of animals that die soon after initial exposure to monensin may show no significant lesions, otherwise hemorrhage and pale areas in the heart with transudation into body cavities may be seen. Evidence of degenerative cardiomyopathy and congestive heart failure may be observed on histopathologic examination. Increased activities of muscle origin enzymes may also be found.The results of controlled studiesand evidence from field reports indicated that the greatest risk of intoxication was upon initial exposure to feed or supplement containing monensin. Feed mistakes and mixing errors were the two most common causes of monensin toxicity in field cases.  相似文献   

19.
Clinical findings in dogs and cats with lead poisoning   总被引:1,自引:0,他引:1  
Over an 11-year period, 68 cases of lead poisoning were diagnosed in dogs and three in cats, accounting for 58.6% and 21.4% of the accidental poisonings in dogs and cats, respectively, presented at the Small Animal Clinic, University of Queensland. Of the dogs, 94% showed alimentary tract involvement and 67.6% central nervous system signs. Blood lead concentrations above 0.3 ppm were considered to indicate toxicity when associated with alimentary tract or central nervous system abnormalities. The percutaneous absorption of lead in dogs is proposed as a factor for intoxication.  相似文献   

20.
This study aimed to identify blood serum lidocaine concentrations in the horse which resulted in clinical signs of intoxication, and to document the effects of toxic levels on the cardiovascular and cardiopulmonary systems. Nineteen clinically normal mature horses of mixed breed, age and sex were observed. Lidocaine administration was initiated in each subject with an i.v. loading dose of 1.5 mg/kg bwt and followed by continuous infusion of 0.3 mg/kg bwt/min until clinical signs of intoxication were observed. Intoxication was defined as the development of skeletal muscle tremors. Prior to administration of lidocaine, blood samples for lidocaine analysis, heart rate, mean arterial blood pressure, systolic blood pressure, diastolic blood pressure, respiratory rate and electrocardiographic (ECG) data were collected. After recording baseline data, repeat data were collected at 5 min intervals until signs of intoxication were observed. The range of serum lidocaine concentrations at which the clinical signs of intoxication were observed was 1.85-4.53 microg/ml (mean +/- s.d. 3.24 +/- 0.74 microg/ml). Statistically significant changes in P wave duration, P-R interval, R-R interval and Q-T interval were observed in comparison to control values, as a result of lidocaine administration. These changes in ECG values did not fall outside published normal values and were not clinically significant. Heart rate, blood pressures and respiratory rates were unchanged from control values. This study establishes toxic serum lidocaine levels in the horse, and demonstrates that there were no clinically significant cardiovascular effects with serum lidocaine concentrations less than those required to produce signs of toxicity.  相似文献   

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