生猪宰后组织器官物理性出血与病理性出血的感官鉴别诊断

在宰后检验中经常会看到生猪的某些组织器官出现出血的现象,其中有些是病理性的.也有很大部分是由运输、屠宰等过程中某些物理性因素造成的.深圳市肉品卫生检验所的检验数据显示:五丰食品(深圳)有限公司清水河肉联厂1991年7月至2001年12月间采用麻电法屠宰的生猪中,皮肤出血的检出率为18%,肌肉出血(暗红肉)的检出率为16%,脂肪出血(红膘)的检出率为20%.肺脏出血的检出率为32%,肾脏出血的检出率为13%,肝脏出血的检出率为17%,脾脏出血的检出率为8%.     

浅谈生猪屠宰检疫和肉品品质检验的要点及其相关性

在生猪屠宰过程中,由官方兽医实施的屠宰检疫和屠宰企业质检人员实施的生猪屠宰产品品质检验是保障肉品质量安全的基本措施。由于屠宰检疫和肉品品质检验流程复杂,且在许多方面相互交织、重叠,致使操作过程中存在职责不清、操作不规范的现象。本文就生猪屠宰检疫和肉品品质检验的要点进行了梳理,并对其异同点进行了分析和总结,为进一步提高基层检疫工作者的屠宰检疫检验水平提供参考。     

生猪屠宰检验检疫监管模式探讨

生猪屠宰检验、检疫是生猪产品质量安全的重要保障,分别由生猪屠宰场和动物卫生监督机构分别派员实施。本文探讨了在畜禽屠宰行业管理职责划转农业部门,检验、检疫由动物卫生监督机构一个部门监管的情况下,理顺生猪屠宰检验、检疫工作。提出合并屠宰检验检疫、企业负责质量并有官方兽医监管、改产品许可为企业许可的设想,以期建立更规范、高效的屠宰检验检疫监管模式。     

生猪屠宰检疫的方法和要点

屠宰检疫不仅是对动物疫病的检测,还是确保动物食品安全,维护人类健康的第一道屏障,所以必须做好生猪屠宰检疫工作。1宰前检验,宰前检验是对即将屠宰的生猪进行的检验。通过宰前检验,能够及时发现可疑病猪,并及时将其从猪群中剔出,避免混入消费市场,危害人类健康,导致疫病传播。     

浅述腾冲市生猪定点屠宰检疫检验

生猪定点屠宰检疫检验是实施猪肉"食品安全"工程的重要措施,通过对腾冲市生猪定点屠宰检疫检验工作进行结合实际的阐述,在介绍腾冲市生猪定点屠宰检疫检验的发展过程、方式方法、操作步骤、结果统计分析及目的等经验方面的检疫检验,给实施生猪定点屠宰检疫检验工作的人员提供参考.     

基层兽医站生猪屠宰检疫检验工作探讨

伴随生猪养殖行业的发展与壮大,养殖户的经营规模也在日益扩大,然而在生猪养殖规模不断扩大的同时,生猪屠宰在检验检疫工作方面也产生了许多问题。如若这类问题无法得到及时的处理,在某种程度上将会增加养殖场中生猪疫病的发生概率。为了能够让生猪养殖产业健康发展,需要高度重视屠宰的检验检疫工作。本文将对基层兽医站的生猪屠宰检验检疫工作展开研究,并据此提出有关建议以供参考。     

生猪屠宰检疫与肉品品质检验异同分析

生猪的屠宰检疫与肉品品质的检验是肉食品行业中最为关键的监督管理工作,二者之间有密切的联系也有一定的区别,国家和政府的相关部门应明确二者的职责划分,对工作内容有严格的规范,进而更好地确保生猪生产加工的安全性。1生猪屠宰检疫与肉品品质检验的区别要想更好地保障肉食品的质量安全,就需要明确生猪屠宰检疫与肉品品质检验的异同之处。首先二者存在内容差异,生猪的屠宰检疫工作由专门的动物检疫机构和专业人员负责,旨在于对动物疾病严格的防控,而肉品的品质检验工作是对肉品的性质以及细菌方面检验,对其有效地监督。     

生猪屠宰卫生检验探讨

《动物防疫法》与《生猪屠宰管理条例》都已实施5年多,国家对生猪等动物实行定点屠宰、集中检疫,为做好动物防疫和我国生猪屠宰检疫工作提供了强有力的法律保障。但是,考虑到历史和现实情况,生猪等动物屠宰检疫一直沿用1959年由农业部、卫生部、对外贸易部、商业部联合颁发的《肉品卫生检验试     

生猪屠宰检疫与摘除"三腺"的重要性

生猪实施定点屠宰、集中检疫 ,不仅对防疫灭病具有重要意义 ,而且直接关系到肉食品的卫生质量 ,是让消费者吃上放心肉的重要保证。生猪屠宰场的集中检疫 ,由宰前检疫和宰后检验两部份组成 ,两者缺一不可。宰前检疫 ,能及时检出病猪 ,特别是对破伤风、伪狂犬病、W病、某些中毒病等一些屠宰以后难于检出的猪病 ,能在屠宰前根据其明显的示病症状 ,被及时发现、检出 ;屠宰后检验 ,是在屠畜解体的情况下 ,对胴体和内脏器官所呈现的病理变化作出综合鉴定。摘除“三腺”,是指屠宰加工和宰后检验时 ,必须把生猪的甲状腺、肾上腺和病变淋巴结全部摘…     

试论屠宰检疫与肉品品质检验的关系

《动物防疫法》规定的屠宰检疫,《生猪屠宰管理条例》规定的肉品品质检验,都是《兽医卫生检验学》、《动物性食品卫生检验》、《肉品科学及肉品卫生检验》等专业著作中提到的专用名词,下面就屠宰检疫、肉品品质检验以及两者之间的关系论述如下：１屠宰检疫包括宰前检疫...     

Abnormal bleeding

Animals with disorders of hemostasis are often presented as emergency patients and, as such, offer a challenge to the attending clinician. This article reviews the basic physiology of hemostasis and laboratory tests used for diagnosis. Guidelines for the evaluation and treatment of patients with bleeding disorders are provided.     

Clinical and laboratory diagnosis of bleeding disorders

The diagnosis of hemostatic abnormalities requires a detailed clinical and laboratory evaluation of the patient. The clinical assessment includes a detailed history and a thorough physical examination. The patient's history may provide clues as to the time of onset of the bleeding tendency, the clinical severity of the abnormality, and the possible contributing role of other disease processes or of drugs. The nature of the bleeding symptoms may provide clues as to the nature of the hemostatic defect. Hemostatic screening tests are invaluable in helping to differentiate between platelet, vascular, coagulation, and fibrinolytic abnormalities. Specific tests, including specific factor assays, platelet aggregometry, and antiplatelet antibody assays are usually required to characterize the exact nature and severity of hemostatic defects.     

Inherited bleeding disorders of dogs and cats

The congenital bleeding disorders of domestic animals usually mimic closely the same disorders in man and are inherited in a similar fashion. Classical haemophilia (haemophilia A, factor VIII deficiency) and haemophilia B (factor IX deficiency) occur in both dogs and cats and are sex-linked conditions. Affected animals are almost always male and heterozygote females are asymptomatic carriers. Offspring of a carrier female have a 50 per cent chance of inheriting the defective X-chromosome and, on average, half of the sons will be affected and half of the daughters will be carriers. Diagnosis of affected animals is confirmed by specific factor assay. Carriers may be identified with a statistical certainty of greater than 80 per cent. Canine von Willebrand's disease is a less severe disorder due to a defect of platelet adhesion. It is an autosomal trait, inherited in most breeds in an incompletely dominant fashion.     

Genetics of equine bleeding disorders

Genetic bleeding disorders can have a profound impact on a horse's health and athletic career. As such, it is important to understand the mechanisms of these diseases and how they are diagnosed. These diseases include haemophilia A, von Willebrand disease, prekallikrein deficiency, Glanzmann's Thrombasthenia and Atypical Equine Thrombasthenia. Exercise-induced pulmonary haemorrhage also has a proposed genetic component. Genetic mutations have been identified for haemophilia A and Glanzmann's Thrombasthenia in the horse. Mutations are known for von Willebrand disease and prekallikrein deficiency in other species. In the absence of genetic tests, bleeding disorders are typically diagnosed by measuring platelet function, von Willebrand factor, and other coagulation protein levels and activities. For autosomal recessive diseases, genetic testing can prevent the breeding of two carriers.     

The influence of the moon on bleeding

The theory of the influence of the stars and in particular of the moon to bleeding was most important in the 17th century; However, a survival of this belief was noted during springtime bleeding or treatment of mare sterility, seldom on other circumstances, in some traditional regions of France from 1930 to 1960. The results presented in the paper are obtained 1990-91 by enquiring of approx. 3.500 French veterinarians graduated 1911-1957.     

Defective gamma-glutamyl carboxylase activity and bleeding in Rambouillet sheep

A flock of Rambouillet sheep was examined because of increased lamb mortality caused by ineffective hemostasis at parturition. Neonatal-affected lambs presented with inadequate hemostasis at the umbilicus, pale mucus membranes, and markedly prolonged activated clotting time. Affected lambs had consistently prolonged 1-stage prothrombin times and activated partial thromboplastin times that supported a defect in the common pathway or defects in both the intrinsic and extrinsic pathway of the coagulation cascade. Decreased activity of vitamin K-dependent procoagulant factors II, VII, IX, and X in male and female lambs suggested either a defect of the hepatic enzyme gamma-glutamyl carboxylase, or vitamin K(1) 2,3 epoxide reductase. Affected lamb hepatic gamma-glutamyl carboxylase activity was markedly decreased compared with that of age- and sex-matched control lambs, while vitamin K(1) 2,3 epoxide reductase and glucose-6-phosphatase activities were similar between an affected and normal lamb. Subcutaneous vitamin K(1) supplementation did not increase vitamin K-dependent procoagulant factor activities in 3 lambs administered vitamin K(1) daily. These data confirm defective gamma-glutamyl carboxylase activity as the cause of impaired coagulation of sheep in this flock. This flock represents the only viable animal model of hereditarily defective gamma-glutamyl carboxylase activity.     

Thrombopathies causing bleeding in a boxer and mixed-breed dog

Hereditary platelet function disorders are clinically characterized by recurrent surface bleeding and prolonged bleeding time, despite normal platelet count and coagulation tests. The authors describe persistent thrombopathies in two young dogs with increased bleeding tendencies but with normal plasma coagulation times and von Willebrand factor (vWf) concentrations. Buccal mucosal bleeding times were prolonged in both dogs. In aggregation studies, platelets underwent only a shape change or minimal aggregation in response to adenosine diphosphate and collagen. Whole-platelet adenine nucleotide concentrations were normal. Electron microscopic evaluation of fibrinogen and vWf binding to the platelets of case no. 1 demonstrated the presence of glycoprotein IIb/IIIa and Ib receptors. Thus, the intrinsic platelet function defects may be different in these two dogs and may likely represent secretion/signal transduction disorders.