Carbofuran poisoning in mallard ducks

Carbofurane, a pesticide from the group of carbamates, has been employed against soil nematodes on a small meadow at the lake of Lugano, Switzerland. On the next morning, the first cases of death involving a total of 19 mallard ducks (Anas platyrhynchos) have been reported. By inhibiting the enzymatic breakdown of the neurotransmitter acetycholine, carbamates lead to excessive activation of the parasympathicus. In addition, paralysis of skeletal muscles is caused by continued stimulation of neuromuscular junctions. Death may occur by asphyxia. In the present case report, the diagnosis of poisoning could be confirmed by the chemical detection of carbofuran in the stomach, blood, muscle and kidney tissue of the affected mallard ducks.     

Influence of dietary calcium on lead poisoning in mallard ducks (Anas platyrynchos)

Forty-five mallard ducks were allotted into 3 dietary groups. Group I was fed pelleted calcium-supplemented corn; group II was fed a pelleted commercial duck ration; and group III was fed cracked corn. Ten ducks of each group were given four No. 4 lead shot via an esophageal tube, and 5 ducks of each dietary group were kept as pair-fed controls. Anorexia and weight loss were most severe in the treated group III ducks. Group III had a maximum reduction in food consumption of 87% followed by a slight improvement in appetite; they lost 35% of their initial body weight. Group I treated ducks had a reduction in food consumption of 64% that eventually returned to the quantities consumed at the start of the experiment; group I ducks lost 18% of their initial body weight. Group II treated ducks maintained healthy appetites during the experiment and had a weight gain of 2% of their initial body weight. The number of ducks that became moribund and were euthanatized differed significantly among the treated groups with 100% of group III, 50% of group I, and 0% of group II treated ducks becoming moribund. All 3 groups of treated ducks had increased protoporphyrin IX concentrations compared with controls. Groups I and III lead-treated ducks had significant (P less than 0.05) reductions in erythrocyte counts, PCV, hemoglobin concentrations, and mean corpuscular hemoglobin concentrations as compared with controls. Group II had reduced hemoglobin concentration and mean corpuscular hemoglobin concentration compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pathogenesis of digestive tract lesions in duck plague.

White Pekin ducklings were inoculated orally with duck plague virus. Tissues from the digestive tract were collected daily after inoculation and examined by light, electron and fluorescent microscopy. There were necrosis and degeneration of stratified squamous epithelium of the esophagus and cloaca, epithelium of intestinal crypt and esophageal submucosal glands, macrophages in the lamina propria, and submucosal fibrocytes and lymphocytes. Submucosal hemorrhages occurred after degeneration and necrosis of lymphocytes, macrophages, fibrocytes and epithelial cells. Viral antigens were detected in all these cells by use of fluorescein-labeled antibodies. With the electron microscope, nucleocapsids were seen in the nuclei, budding through the inner nuclear membrane; enveloped virions were present in cytoplasmic vacuoles of macrophages, epithelial cells and fibrocytes. In lymphocytes, nucleocapsids were also in the nuclei, but karyorrhexis and cytolysis occurred before viral maturation was completed.     

Treatment of lead poisoning in wild geese.

Twenty-seven wild geese (Anser albifrons) suffering from lead poisoning caused by ingestion of lead shot were treated with disodium calcium ethylenediaminetetraacetate. The concentration of lead in blood ranged from 0.4 to 23.0 micrograms/ml, with a mean concentration of 5.6 micrograms/ml. In 22 of the birds, 1 to 48 lead pellets (mean, 10.5 pellets/bird) were seen on radiographs of their gizzards. Eleven of 27 birds recovered 3 to 8 weeks after the initiation of treatment. In the birds that recovered, the lead pellets were rapidly eroded as the birds recovered their appetites in response to treatment, and disappeared radiographically between treatment days 17 and 52. The birds that did not survive died within 4 weeks, despite decreased concentrations of lead in blood. Of these 16 birds, 15 had radiographic evidence of impaction of the proventriculus at the first examination and no evidence of resolution of the impaction at the time of death. In contrast, only 2 of the 11 geese that recovered had impaction of the proventriculus at the time of admission. Thus, the condition of the proventriculus seems to be the first consideration to evaluate in the prognosis of lead poisoning in geese.     

Pathogenesis of duck plague in the bursa of Fabricius, thymus, and spleen.

White Pekin ducks were inoculated orally with duck plague virus and killed at 24-hour intervals after inoculation. Spleen, thymus, and bursa of Fabricius were collected and examined by light, fluorescent, and electron microscopy. Necrosis of lymphocytes occurred in the bursa of Fabricius, thymus, splenic periarteriolar lymphoid sheath (T lymphocytes), and splenic germinal centers (B lymphocytes). Viral nucleocapsids were present in the karyoplasm of lymphocytes, but these cells necrotized before virions were formed. Periarteriolar reticular sheath cells and sinusoidal lining cells in the spleen, epithelial cells in Hassall's corpuscle of the thymus, epithelial cells between the cortex and medulla of the follicles in the bursa of Fabricius, and macrophages in all 3 tissues contained nucleocapsids in the nuclei and virions in cytoplasmic vacuoles before necrosis occurred.     

Chronic lead poisoning in horses

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.     

丰县地区肉鸭慢性食盐中毒的诊治

最近丰县有不少的养殖户反映他们的肉鸭经常有饮水偏多、拉水样稀粪、运动失调、有时出现瘫痪、头颈弯曲、胸腹朝天、仰卧挣扎,最后衰竭死亡,用药无明显疗效等情况,最后诊断为慢性食盐中毒.     

鸭肉毒梭菌中毒的诊治

2008年8月中旬,新民市高某从一倒闭养鸭场购得90日龄鸭1000只,由于事先没有准备,放入村头一个约2万m2的大坑中,大量鸭出现死亡,死亡率达87.4%.通过流行病学调查、临床症状和动物试验,确诊为肉毒梭菌中毒,现将诊治情况报告如下.     

荧粉致蛋鸭中毒的病理学观察

鞭炮生产原料荧粉造成300多只蛋鸭中毒死亡。死亡率达到60％，持续时间一个多月。对死亡鸭各脏器的组织病理检查结果表明，肺因异物沉积呈出血性变化；肝实验坏死，并且枯否氏细胞明显增生，内有黑色颗粒；肾出现广泛的肾小管变性坏死。