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奶牛产后瘫痪的病因临床症状治疗及预防措施奶牛产后瘫痪是指奶牛在分娩后出现运动障碍的病症。
其病因复杂，包括营养不良、钙磷代谢失调、神经损伤等。
产后瘫痪临床症状明显，主要表现为四肢无力、行走困难、下垂耳朵等。
针对奶牛产后瘫痪的病情，可以采取多种治疗和预防措施。
治疗：1. 营养治疗：确保产牛饲料的充足、适宜，增加适宜的能源和蛋白质摄入量，保证产牛的体重不下降，防止因为营养不良引起的产后瘫痪。
2. 补钙疗法：根据兽医师的建议，给予奶牛适当的钙补充剂，加强钙磷代谢，可以采用静脉给药或饲喂高钙饲料。
3. 物理治疗：适当的运动治疗可以帮助奶牛恢复运动功能。
可以用吊索扶起奶牛四肢，帮助其站起来。
4. 药物治疗：根据兽医师的处方，给予奶牛适当的药物，如激素类药物，对于产后瘫痪有一定的促进作用。
预防：1. 合理的饲养管理：建立合理的饲养管理制度，确保奶牛的饲料营养均衡，保证奶牛充分的休息和活动。
2. 分娩期间的监护：兽医师应在奶牛分娩期间进行密切监护，确保产犊过程顺利进行，避免可能导致神经损伤的情况发生。
3. 预防钙磷代谢失调：适当调整饲喂奶牛饲料中的钙磷比例，合理补充钙磷，以维持钙磷代谢平衡。
4. 提供适宜的运动和活动空间：奶牛在分娩后应该有足够的运动和活动空间，避免长时间站立或无法正常活动而引发产后瘫痪。
奶牛产后瘫痪是一种常见的疾病，病因复杂。
在治疗方面，需要根据具体情况采取综合措施，包括营养治疗、补钙疗法、物理治疗和药物治疗等。
在预防方面，合理的饲养管理、分娩期间的监护、钙磷代谢调节和提供适宜的运动空间都是非常重要的预防措施。
为了确保奶牛的健康和生产效益，养殖户应该加强对奶牛产后瘫痪的预防和治疗的认识，及时采取相应的措施，保障奶牛的健康和生产性能。
奶牛产后瘫痪的发病因素临床症状鉴别诊断和防治奶牛产后瘫痪是奶牛在产后因一些原因导致的疾病，严重影响了奶牛的生产性能和健康状况。
本文将从产后瘫痪的发病因素、临床症状、鉴别诊断和防治进行详细介绍。
一、发病因素1. 营养不良：奶牛在产后需要大量的营养来恢复体力和生产，如果长时间缺乏必要的营养元素，就容易导致体力不足和产后瘫痪的发生。
2. 饮水受限：饮水受限也是导致奶牛产后瘫痪的原因之一，因为水分的摄入不足会导致体内代谢产物不易排出，进而引起产后瘫痪。
3. 环境胁迫：奶牛在产后需要一个干净、安静、通风良好的环境来休息，如果环境不良，容易导致奶牛产后瘫痪的发生。
4. 产后促产素分泌不足：促产素在产后是非常重要的激素，它可以促进子宫收缩和恢复，如果产后促产素分泌不足，就可能导致产后瘫痪的发生。
二、临床症状1. 走动困难：产后瘫痪的奶牛走动时会非常困难，常常蹒跚而行，有时甚至无法站立。
2. 营养不良：产后瘫痪的奶牛常常出现食欲不振、消瘦、体温升高等症状。
3. 阴道分泌物异常：有时产后瘫痪的奶牛会出现阴道分泌物异常的情况，甚至呈现脓性分泌物。
4. 情绪不佳：产后瘫痪的奶牛常常情绪不佳，表现为食欲不振、暴躁等症状。
三、鉴别诊断产后瘫痪的临床症状与其他疾病的症状有一定的相似之处，需要进行鉴别诊断。
1. 鉴别产后瘫痪和低血钙症：低血钙症是奶牛产后的常见疾病之一，其临床症状与产后瘫痪相似，容易混淆。
但通过检测血钙水平和维生素D水平可以确定诊断。
2. 鉴别产后瘫痪和感染性疾病：有时，奶牛产后瘫痪的症状与感染性疾病相似，需要通过检测体温、白细胞计数等指标来进行鉴别诊断。
四、防治1. 营养保障：产后瘫痪的防治首先要做好营养保障，给予奶牛充足的高质量饲料，保证产后的营养需求。
2. 饮水保障：保证奶牛产后充足的饮水量，有利于促进体内代谢产物的排出，减少发生产后瘫痪的几率。
3. 良好的生产环境：给予奶牛一个安静、通风良好、干净的生产环境，有利于促进奶牛的康复。
奶牛产后瘫痪的发病因素临床症状鉴别诊断和防治奶牛产后瘫痪是指奶牛在分娩后出现下肢麻痹和无法正常站立的病症。
产后瘫痪是奶牛常见的疾病之一，如果不及时诊断和治疗，将会导致奶牛的生产性能下降和经济损失。
本文将从发病因素、临床症状、鉴别诊断和防治措施四个方面进行介绍。
一、发病因素：1. 难产：奶牛分娩过程中难产是常见的原因之一，难产会导致奶牛子宫和盆腔受伤，进而引发产后瘫痪。
2. 脑部疾病：如脑炎、脑血栓、脑膜炎等，这些疾病会导致奶牛神经系统受损，引发产后瘫痪。
3. 饮食不当：产后饲食不足或饲料中缺乏维生素、矿物质等营养元素，会导致奶牛体力不佳，减弱肌肉力量，易引发产后瘫痪。
4. 胸腔腹腔手术：如剖宫产、瘤胃切除术等，这些手术会对奶牛的组织和器官造成损伤，引发产后瘫痪。
5. 粉刺瘤病：这是一种由细小颗粒性病毒引起的传染病，会导致奶牛产后病毒感染，进而引发产后瘫痪。
二、临床症状：1. 麻痹：奶牛产后瘫痪的主要症状是后肢麻痹，奶牛无法正常行走和站立，有时甚至不能翻身。
2. 筋膜反射消失：在正常情况下，奶牛后肢筋膜反射是存在的，而产后瘫痪时，筋膜反射会消失。
3. 病情加重：产后瘫痪的病情会逐渐加重，奶牛无法自行恢复，需要及时治疗。
4. 无自觉咀嚼：奶牛产后瘫痪时，常常出现无法自觉咀嚼的情况，食欲下降。
三、鉴别诊断：1. 分娩问题：需要通过产后麻痹的症状来判断是否与分娩过程中的损伤有关。
2. 脑部疾病：通过体检和相关检查，判断是否有脑部疾病的存在。
3. 营养问题：通过饲养管理和饲料分析，判断是否与饮食不当有关。
4. 手术史：检查奶牛是否有胸腔腹腔手术史，以排除手术造成的损伤。
5. 病毒感染：通过病原学检查，判断是否与病毒感染有关。
四、防治措施：1. 补充营养：对于由于饮食不当引起的产后瘫痪，需要补充营养，提高奶牛体力，可以通过增加粗饲料和添加维生素、矿物质等饲料来实现。
2. 应激管理：分娩是一种应激反应，为了减少奶牛在分娩过程中的受损，可以采取适当的应激管理措施，如提供相对安静和舒适的分娩环境，减少外界干扰。
奶牛产后瘫痪的病因临床症状治疗及预防措施1. 引言1.1 奶牛产后瘫痪简介奶牛产后瘫痪是奶牛在产后出现的一种常见疾病，也称为产后瘫痪、产后躯体瘫痪或产后肌无力。
这种疾病主要发生在奶牛产后的数周内，特点是奶牛出现腰腿无力、站立困难、无法正常行走等症状。
产后瘫痪给奶牛的生产和生活带来了很大的困扰，严重影响了奶牛的生产效率和健康状况。
产后瘫痪的发生与产后奶牛体内矿物质代谢异常、机体能量供应不足、产后管理不当等因素有关。
在产后营养不良、劳累过度或腰腿部受伤的情况下，更容易导致奶牛发生产后瘫痪。
产后瘫痪的症状主要表现为腰腿无力、下垂等，严重的病例甚至无法站立。
治疗方法主要包括提供充足的营养、行动不便的奶牛应得到适当的照顾，并及时进行药物治疗以减轻症状。
预防措施主要包括产后管理的规范、保证奶牛充足的营养供应等。
通过对产后瘫痪的认识和治疗，可以有效预防并减少这种疾病对奶牛的危害，提高奶牛的生产效率和健康水平。
这对于奶牛养殖业的发展具有重要意义。
2. 正文2.1 病因奶牛产后瘫痪是一种常见的产后疾病，严重影响了奶牛的生产能力和健康状况。
产后瘫痪的病因主要包括以下几个方面：1. 营养不良：奶牛产后需要大量的能量和营养来支持产奶和恢复身体的过程。
如果奶牛在产后的饲养管理中营养不良，导致体内营养缺乏，就容易导致产后瘫痪的发生。
2. 钙和磷的代谢异常：产后奶牛在分娩后体内的钙和磷需要迅速调整到正常水平，如果无法及时调整，就容易导致产后瘫痪。
3. 生理问题：有些奶牛可能有生理问题或遗传问题，导致其在产后易患产后瘫痪。
4. 过度疲劳：产后奶牛如果疲劳过度或受到过度的应激，也容易诱发产后瘫痪的发生。
奶牛产后瘫痪的病因是多方面的，需要在饲养管理上加强营养供给、注意钙磷的平衡、预防过度疲劳等方面进行综合管理，以降低奶牛产后瘫痪的发生率。
2.2 临床症状奶牛产后瘫痪的临床症状主要包括以下几个方面：1. 运动障碍：患有产后瘫痪的奶牛在站立和行走时表现出明显的困难，甚至无法站立或行走。
奶牛产后瘫痪的发病因素临床症状鉴别诊断和防治奶牛产后瘫痪是指在奶牛产后发生的一种神经肌肉疾病，其主要症状是奶牛无法站立和行走。
产后瘫痪的发病因素有很多，包括以下几个方面：1. 酸中毒：在产犊后，奶牛的体内产生大量的乳酸，如果不能迅速排出体外，就会导致酸中毒，进而影响神经肌肉的正常功能。
3. 产犊损伤：在奶牛产犊时，可能会因为胎儿体型过大、胎儿在产道中滞留等原因导致产道受损，进而影响到神经的传导和肌肉的发育。
4. 营养不良：在奶牛产后，由于饲养条件或者饲料供应不足，奶牛的体内可能会出现营养不良，从而导致肌肉无力或者神经功能受损。
产后瘫痪的临床症状主要包括以下几个方面的表现：1. 奶牛无法站立或者部分无法站立，只能趴着或者侧躺。
2. 奶牛行走困难，只能用前腿或者后腿一侧进行移动。
3. 奶牛的背部肌肉松弛，不能够支撑起身体。
4. 奶牛食欲不振，可能出现腹泻和消化不良等问题。
5. 奶牛全身乏力，无精打采，可能出现发热和抽搐等症状。
为了进行准确的诊断和治疗，可以根据以下几个方面进行鉴别诊断：1. 体检：通过仔细观察奶牛的站立和行走情况，检查肌肉的紧张程度，以及观察有无其他异常症状。
2. 血液检查：可以通过血液检查来确定奶牛的酸中毒程度、血钙浓度和其他相关指标，从而进一步确定产后瘫痪的原因。
3. X线检查：如果怀疑产道受损和神经损伤，可以进行X线检查来确定。
1. 补充营养：在奶牛产后，需要给予足够的饲料，尤其是丰富的蛋白质和钙质，以帮助奶牛恢复体力和肌肉功能。
2. 矫正姿势：对于有痉挛和畸形的奶牛，可以进行适当的矫正，帮助奶牛恢复正常的姿势。
3. 康复训练：通过物理疗法和康复训练，可以帮助奶牛恢复肌肉的力量和协调性。
4. 管理调整：对于有产道受损的奶牛，需要调整产后的管理方法，预防再次发生产后瘫痪。
产后瘫痪是奶牛产后易发生的一种疾病，其发病因素复杂多样。
对于出现瘫痪症状的奶牛，需要及时诊断和治疗，以减少损失和提高奶牛的生产能力。
奶牛产后瘫痪的病因临床症状治疗及预防措施奶牛产后瘫痪（postpartum paresis, 大女儿肌消退症）是一种常见的奶牛疾病，主要发生在产后72小时内。
奶牛产后瘫痪的发病机制是由于低血钙（低钙血症）引起的神经肌肉功能紊乱。
病因：奶牛在分娩过程中，会大量失去血液与体内储备的矿物质，特别是钙。
如果奶牛无法及时从饲料中摄取足够的补充，血液中的钙含量就会明显下降，引发低钙血症。
低钙血症会导致奶牛神经和肌肉功能紊乱，从而引发产后瘫痪。
临床症状：- 奶牛无法正常站立或移动- 吃喝减少，食欲不振- 乳量减少，甚至停产- 收缩性慢，容易感染- 角膜混浊，严重则角膜溃烂治疗措施：产后瘫痪是一种紧急情况，需要及时治疗。
常用的治疗措施包括：- 静脉输液：通过静脉给予高钙液体以纠正低钙血症，并维持奶牛的水分和营养平衡。
- 补钙治疗：可以通过口服或肌肉注射补充钙质，纠正低钙血症。
但需要正确掌握补钙剂的剂量与用法，避免引发钙磷代谢紊乱。
- 其他支持治疗：如保持奶牛的床铺干燥卫生，为其提供适当饲料以满足其营养需求。
预防措施：- 合理饲养管理：提供高品质的饲料，确保奶牛能够摄取足够的钙和矿物质。
适量补充维生素D，以促进钙的吸收和利用。
- 产前营养调整：在分娩前提前补充奶牛的钙和矿物质储备，避免营养不良引起的低钙血症。
- 合理繁殖管理：维持奶牛的孕期合理，避免产后瘫痪的发生。
- 规律运动：适量的运动会促进奶牛骨骼健康和钙的吸收。
奶牛产后瘫痪是一种常见且严重的疾病，但通过合适的预防措施和及时的治疗，可以有效地防止和控制这种疾病的发生和蔓延。
奶牛产后瘫痪的发病因素临床症状鉴别诊断和防治奶牛产后瘫痪是指奶牛在分娩后出现腰骶部或后肢不能正常运动的症状。
产后瘫痪是奶牛繁殖管理中的一个常见疾病，严重影响其生产性能和经济效益。
本文将介绍奶牛产后瘫痪的发病原因、临床症状鉴别诊断和预防治疗策略。
一、发病因素1. 饲养管理不当：饲喂营养不均衡、缺乏微量元素等，导致奶牛体质弱，易发生瘫痪。
2. 分娩问题：难产、窝饲分娩和娴熟分娩等问题均与产后瘫痪的发生有关。
3. 繁殖问题：孕期疾病、胎位异常等问题可能引起产后瘫痪的发生。
4. 冷应激：寒冷环境及寒冷季节增加了奶牛产后瘫痪的发生。
二、临床症状鉴别诊断1. 发病早期：奶牛出现后肢跷蹄步态、行走不稳，甚至出现躺倒不起的症状。
2. 发病中期：奶牛完全瘫痪，不能站立，只能侧卧。
3. 发病后期：奶牛四肢抽搐，出现肢体无力和感觉减退的症状。
根据临床症状和病史，通常可以鉴别出奶牛是否患有产后瘫痪。
但为了确诊，建议牧场进行相关检查，如血液检验、胎盘检查等。
三、防治策略1. 预防措施：加强繁殖管理，保证孕期营养需求，及时处理产妇病，注意分娩操作，防止难产。
保证牛舍的温暖干净，防止奶牛受冷应激。
2. 饲养管理：合理饲喂，保证奶牛的全面营养。
特别是要注意补充维生素、微量元素等，提高奶牛的免疫力。
3. 早期治疗：产后瘫痪奶牛需要及时给予治疗。
可以采用药物治疗、钙补充疗法等，促进奶牛恢复运动功能。
4. 康复治疗：奶牛康复阶段，可以进行理疗和运动康复，帮助奶牛恢复正常生活。
奶牛产后瘫痪是一种常见疾病，对奶牛的健康和生产性能有严重影响。
通过加强饲养管理，预防措施和早期治疗，可以有效减少产后瘫痪的发生，提高奶牛的生产效益。
奶牛产后疾病发病率标准
乳房炎是奶牛产后常见的疾病，其发病率标准通常在5%左右。
乳房炎会导致奶牛乳房肿胀、乳汁产量减少，严重的话甚至会影响
奶牛的生产性能。
产后衰弱是另一个常见的问题，尤其是在繁殖高产奶牛时更为
突出。
其发病率标准通常在10%左右。
产后衰弱会导致奶牛产后恢
复能力减弱，容易受到其他疾病的侵害。
产后脱水和产后酮症也是产后常见的疾病，其发病率标准在5%
左右。
产后脱水会导致奶牛体内水分丧失过多，影响正常生理功能；而产后酮症则会导致奶牛体内代谢紊乱，影响产奶量和质量。
然而，需要指出的是，这些发病率标准仅供参考，实际情况还
会受到诸多因素的影响，包括饲养管理、饲料营养、环境条件等。
因此，为了降低奶牛产后疾病的发病率，养殖户需要加强对奶牛的
管理和护理，保证其健康和生产性能。
奶牛酮病的发生原因临床症状和防治措施【摘要】奶牛酮病是奶牛在产后容易发生的一种代谢性疾病，常见于高产奶牛。
该病的发生原因主要包括产后应激、饲养管理不当、饲料营养不均衡等因素。
临床症状表现为食欲不振、腹泻、体重下降、乳量减少等。
为了防治奶牛酮病，饲养管理者应注意提供充足的营养、保持良好的饲养环境，定期检查奶牛的体重和产奶量等。
对于患有奶牛酮病的奶牛，及时进行药物治疗、调整饲料配方，帮助奶牛恢复健康。
只有加强对奶牛酮病的重视，提高饲养管理水平，才能有效预防和控制这种常见的代谢性疾病，保障奶牛的健康和生产。
【关键词】奶牛酮病、发生原因、临床症状、防治措施、重视。
1. 引言1.1 奶牛酮病简介奶牛酮病，又称为乙酰乳酸血症或酮症，是一种常见的代谢性疾病，主要发生在高产奶牛身上。
这种疾病通常在产后两到三周内发生，其主要病因是由于高产奶牛体内葡萄糖供应不足，导致脂肪代谢过程中产生的乙酰乳酸和酮体在血液中积聚。
这些物质的积聚会导致奶牛产生一系列临床症状，比如食欲不振、体温升高、乳品质下降等。
在严重的情况下，奶牛甚至会出现严重的脱水和体重下降。
奶牛酮病对奶牛的生产和健康造成了严重影响，因此及早发现并采取有效的防治措施对于奶牛的生产性能和生命健康非常重要。
预防奶牛酮病的关键在于合理的饲养管理和营养调控，包括合理的饲料配比、适当的运动和充足的饮水等。
及时发现奶牛酮病的临床症状，并采取有效的治疗措施也至关重要。
通过加强对奶牛酮病的认识和重视，可以有效降低奶牛的发病率，保障奶牛的健康和生产性能。
2. 正文2.1 发生原因奶牛酮病是奶牛常见的一种新陈代谢性疾病，其发生原因主要有以下几个方面：1. 饲养管理不当：奶牛在产后和哺乳期的能量需求相对较高，如果饲料配比不合理或者喂养方式不当，容易导致奶牛体内葡萄糖供应不足，从而引发酮病发生。
2. 过度瘦身：有些奶农为了追求奶牛高产，会在产后过度控制奶牛的饲料量，导致奶牛体内能量储备不足，容易诱发酮病。
奶牛产后瘫痪的病因临床症状治疗及预防措施奶牛产后瘫痪，是指奶牛在产后因为身体虚弱或其他原因，导致下半身瘫痪的病症。
这种疾病对奶牛的生产和生活造成了很大影响，因此我们需要了解产后瘫痪的病因、临床症状、治疗和预防措施。
一、病因1. 营养不良奶牛在产后需要大量的营养来恢复身体，如果奶牛的营养摄入不足，容易导致代谢紊乱，从而引发产后瘫痪。
2. 生产劳累奶牛在分娩过程中需要承受很大的劳累，如果分娩过程中受到了损伤或者过度劳累，也容易导致产后瘫痪的发生。
3. 场所环境如果奶牛的生活环境不合理，例如常年潮湿、通风不良等，这些环境因素也会影响奶牛的健康，增加了产后瘫痪的发生风险。
二、临床症状1. 下半身无力奶牛在产后瘫痪后，下半身会出现无力的症状，无法站立或行走。
2. 食欲减退产后瘫痪的奶牛常常食欲减退，进食量明显减少，导致营养不良。
3. 体温升高瘫痪的奶牛由于无法行走，体温调节能力下降，容易出现体温升高的情况。
4. 精神状态差产后瘫痪的奶牛常常表现出精神状态差、消沉等情况，甚至出现情绪波动。
三、治疗1. 提供适当的营养对于患有产后瘫痪的奶牛，首先需要保证其获得足够的营养，可以饲喂高品质的青贮料、浓缩饲料等，以满足其身体的营养需求。
2. 给予良好的护理对于瘫痪的奶牛，需要给予良好的护理，如保持场所清洁干燥，定期为奶牛梳理毛发，定期清洗奶牛身体等，保证奶牛的健康。
3. 经常转移体位为了避免因长时间处于同一体位而加重瘫痪的情况，需要定时将奶牛转移体位，帮助其保持适当的血液循环。
4. 及时治疗一旦发现奶牛出现了产后瘫痪的症状，需要及时请兽医进行诊断和治疗，不能拖延。
四、预防措施1. 合理饲喂在奶牛分娩后，需要合理增加其饲喂，满足其身体对营养的需求，防止因为营养不良而引发产后瘫痪。
2. 生产管理在奶牛分娩时，需要提供良好的生产环境和产后护理，避免因为劳累或者环境因素导致产后瘫痪的发生。
3. 定期体检定期为奶牛进行体检，及时发现患病情况，并进行预防和治疗。
奶牛产后瘫痪的发病因素临床症状鉴别诊断和防治奶牛产后瘫痪是指在产后一段时间内，奶牛出现运动障碍，无法自行站立起来的疾病。
产后瘫痪是奶牛常见的产后并发症之一，严重影响了奶牛的生产性能和健康状况。
本文将介绍奶牛产后瘫痪的发病因素、临床症状鉴别诊断和防治措施。
一、发病因素1.营养失衡：产后奶牛需要摄取大量的营养物质，特别是能量和钙，以保证产后机体的恢复和乳量的正常产出。
如果营养摄入不足，特别是钙摄入不足，会导致奶牛产后低血钙，进而引起产后瘫痪。
2.产后应激：奶牛在分娩后会经历一段时间的应激期，特别是在初产母牛中更加明显。
由于分娩的过程中伴随着强烈的疼痛和应激反应，加之分娩后新生儿的哺乳和照料需求，会导致奶牛产后应激反应过度，进而影响其运动功能。
3.疾病感染：分娩是奶牛抵抗力下降的一个重要时刻，容易感染各种病原体。
如果奶牛在分娩后受到细菌、病毒、寄生虫等病原体的感染，会引起免疫系统的反应，进而导致产后瘫痪的发生。
4.运动过度：分娩后奶牛需要恢复体力，但如果过度运动，特别是在分娩后疲劳或躁动时，容易导致肌肉疲劳和酸化，加重奶牛的运动障碍。
二、临床症状鉴别诊断1.产后瘫痪的早期症状：在分娩后的几天内，奶牛常常会出现食欲不振、运动减少、蹄蹂躏、步态不稳等早期症状。
有时奶牛可站立但无力走动，仅能进行短距离的行走。
2.产后瘫痪的进展症状：如果早期症状得不到及时控制，奶牛的瘫痪症状会逐渐加重。
奶牛无法自主站立，躺在地上无力、无助地挣扎，四肢僵硬，甚至无法动弹。
尿液和粪便的排出也会受到影响。
3.其他症状：产后瘫痪的奶牛还可能出现新生儿抚育能力下降、乳量减少、发热、饮水减少、体温下降等症状。
对于以上症状的奶牛，通过观察临床症状可以初步判断是否为产后瘫痪，但还需要进一步的实验室检查和诊断才能明确诊断。
三、防治措施1.营养调整：产后奶牛应从分娩前的高产期开始，逐渐增加饲料和营养素的摄入，特别是需要注意增加钙的摄入。
可以通过饲料补充、添加饲料中的矿物质等方式来增加钙的摄入。
奶牛产后瘫痪的发病因素临床症状鉴别诊断和防治
奶牛产后瘫痪是奶牛在产后出现的一种神经肌肉疾病，通常发生在产后的第一周。
该
病的发病因素包括营养不良、低血钙、低血磷、低血镁、骨质疏松、血钙磷失衡、胃失活等。
临床症状方面，产后瘫痪的奶牛会表现出以下一些特征：患牛运动机能明显减弱，体
温升高，食欲减退，并出现不适的呼吸。
患牛会出现四肢的无力，行走困难，站立时间减少，严重的患牛甚至会出现无法站立。
患牛的肠胃功能也会出现异常，常伴随着腹胀、粪
便变硬、无乳等症状。
一些患牛还会出现神经退行性病变的症状，如牙齿咬合力度减弱、
听力减退等。
在鉴别诊断方面，研究人员可以通过观察奶牛的临床症状来进行初步的鉴别。
对于无
法站立的奶牛，可以通过检查胃和结肠的蠕动情况来判断是否为产后瘫痪。
通过检查奶牛
的牙齿和听力状况，可以排除其他神经肌肉疾病，从而进一步确诊产后瘫痪。
在防治方面，对于奶牛的健康管理是至关重要的。
畜牧户需要提供饲料的全面营养，
包括蛋白质、钙、磷、镁等重要营养素。
畜牧户还应该注重奶牛的饲养环境，保持奶牛舒
适和安静的环境，避免过度劳累和精神紧张。
在治疗方面，畜牧户可以在兽医的指导下进
行营养补充和药物治疗，以帮助奶牛恢复运动机能。
奶牛产后瘫痪是一种常见的神经肌肉疾病，其发病因素主要包括营养不良、低血钙、
低血磷等。
临床症状表现为运动机能减弱、四肢无力、肠胃功能异常等，鉴别诊断主要通
过观察临床症状和进行相关检查。
预防和治疗方面，需要注意奶牛的饲养环境和营养补充，同时在兽医的指导下进行治疗。
奶牛产后瘫痪的病因临床症状治疗及预防措施
奶牛产后瘫痪是一种常见的产后疾病，其主要病因包括脊髓炎、低钙血症和低磷血症等。
临床症状：
1. 运动障碍：产后瘫痪的奶牛常出现运动障碍，包括无法站立、跛行、踉跄等现象。
2. 腱反射减弱：奶牛的腱反射在产后瘫痪时常会减弱或消失。
3. 食欲减退：奶牛在受到产后瘫痪的影响时，常会出现食欲减退的情况。
4. 体温升高：由于运动障碍及其他因素，奶牛常常出现体温升高的情况。
治疗：
1. 质子泵抑制剂：对于由于低钙血症引起的产后瘫痪，可以给予质子泵抑制剂进行治疗，以减少胃酸分泌，促进钙的吸收。
2. 补钙治疗：对于由于低钙血症引起的产后瘫痪，可以通过给予补钙治疗来纠正低钙血症。
常见的治疗方法包括给予静脉补钙或口服补钙。
3. 补磷治疗：对于由于低磷血症引起的产后瘫痪，可以通过给予补磷治疗来纠正低磷血症。
常见的治疗方法包括给予口服补磷或食物添加剂。
4. 止痛剂：对于产后瘫痪较严重的奶牛，可以给予适当的止痛剂来缓解疼痛。
预防措施：
1. 合理饲养管理：加强对奶牛的饲养管理，保证奶牛的营养摄入量和品质，避免营养不均衡。
2. 增加运动量：给予奶牛适当的运动量，促进奶牛的肌肉和骨骼发育，增强体质。
3. 定期检查：定期进行奶牛的健康检查，早期发现产后瘫痪的症状，及时给予治疗。
4. 饲喂添加剂：根据奶牛的需要，适当地添加钙、磷等营养补充剂，维持奶牛的体内平衡。
产后瘫痪是一种严重影响奶牛产后健康的疾病，及时的诊断和治疗对于奶牛的康复和生产性能的恢复非常重要。
通过加强预防措施和科学管理，可以有效减少产后瘫痪的发生。
奶牛产后瘫痪的发病因素临床症状鉴别诊断和防治【摘要】奶牛产后瘫痪是奶牛在产后发生的一种瘫痪现象，影响了奶牛的生产和健康。
产后瘫痪的发病因素包括营养不良、钙缺乏、运动不足等因素。
临床症状主要表现为站立困难、行走异常等。
与其他疾病相比，需要通过详细的体检和实验室检查来进行鉴别诊断。
预防和治疗方面，关键在于提供良好的营养、增加运动量和定期检查。
综合管理策略包括合理的饲养管理、定期体检和及时治疗，以确保奶牛的健康和生产水平。
通过进行综合管理，可以有效预防和控制奶牛产后瘫痪的发生，保障奶牛的生产和健康。
【关键词】奶牛产后瘫痪、发病因素、临床症状、鉴别诊断、防治措施、综合管理策略1. 引言1.1 产后瘫痪的概述产后瘫痪是奶牛在产后发生的一种疾病，主要表现为下肢无力、无法站立和行走。
这种疾病给奶牛的生产和健康带来了严重影响，严重程度因个体而异，可导致生产性能下降和脂肪肝等并发症的发生。
产后瘫痪的发病率在奶牛中并不高，但一旦发生就需要及时有效地进行治疗。
产后瘫痪的发病原因多种多样，如胎儿过大、难产、生产过程中受伤等。
临床上常见的症状包括下肢无力、站立困难、体温升高、食欲不振等。
在与其他疾病的鉴别诊断中，需要与酮症、酸中毒等疾病进行区分。
预防产后瘫痪的关键在于科学管理，包括合理饲养、产前检查、生产过程的护理等。
综合管理策略应包括提高营养水平、加强体检监测、及时治疗和预防难产等措施，以保障奶牛的生产和健康。
2. 正文2.1 产后瘫痪的发病因素奶牛产后瘫痪是一种常见的产后疾病，其发病因素主要包括以下几点：1. 营养不良：奶牛在产后需要大量的营养来满足产奶和身体恢复的需要，如果食物中缺乏必要的营养素，如蛋白质、维生素等，就容易导致奶牛体力不支，从而引发产后瘫痪。
2. 运动不足：产后奶牛由于需要大量休息来恢复体力，但长时间的卧床休息也容易造成肌肉的松弛和萎缩，从而使奶牛丧失了正常行走的能力。
3. 胎产困难：如果奶牛在产犊过程中遇到胎产困难并需要手术干预或外力助产，就会增加其产后瘫痪的发病风险。
奶牛产后瘫痪的发病因素临床症状鉴别诊断和防治奶牛产后瘫痪是一种常见的疾病，主要由于产后营养不良、饮水不足、生理调节失衡等多种因素引起。
该疾病严重影响了奶牛的健康和生产性能，因此对该病的防治十分重要。
发病因素1. 营养不良：奶牛在产后需要大量的营养来支持身体恢复和奶量的增长，如不能摄食足够的饲料，会导致能量、蛋白质、矿物质等多种营养缺乏，从而引发产后瘫痪。
2. 水分不足：奶牛产后需要大量饮水，而水分不足会导致身体内部的代谢失衡，从而影响奶牛的生理健康和产量。
3. 生理调节异常：奶牛在生理调节方面容易受到环境、饮食等因素的影响，如产后子宫内膜不完全清理，会导致体内荷尔蒙分泌失衡，从而引起产后瘫痪。
临床症状产后瘫痪的临床症状表现为：奶牛一侧蹄部及下肢无力，不能站立行走，甚至不能下蹲或稍作动作便会跌倒。
同时，其食欲降低、睡眠时间延长、奶量减少等生产表现也会受到影响。
鉴别诊断1. 水肿型产后瘫痪：奶牛双侧蹄部和四肢出现水肿，腹部膨胀，体重大幅上升。
2. 萎缩型产后瘫痪：奶牛下肢强度和膝关节角度都有不同程度减小，双后肢因度数不同而呈现交叉状。
3. 急性脑部疾病引起的产后瘫痪：奶牛会出现头痛、眩晕、神志不清等症状。
防治方法1. 加强营养管理：保证奶牛产后摄食充足的饲料，提高日粮中营养元素的含量，如蛋白质、钙、磷等，以支持其体内代谢及生产恢复。
2. 加强水分管理：奶牛产后需要充足的清水以支持其生物代谢和水分需要，因此，应该保证其饮水的可及性，并进行周期性的饮水观察。
3. 加强环境管理：保证奶牛的舒适性和卫生性，注意通风、排泄物清理和病原体的隔离与治疗。
综上所述，奶牛产后瘫痪的发病因素和症状都比较复杂，防治的方法也比较多样化，但综合管理包括饮食、水分和环境三方面，是防治产后瘫痪的根本措施。
lumen of most dairy cattle in the first two weeks after parturition in many situations, althoughin some countries the frequency is lower [2-6]. Although many cows eliminate these bacteriaduring the five weeks after parturition, in 10 to 17 % of animals persistence of bacterial infectioncauses uterine disease clinically detectable by physical examination [7,8]. The presence ofbacteria in the uterus causes inflammation, histological lesions of the endometrium, delaysuterine involution and perturbs embryo survival [9-11]. In addition, uterine bacterial infection,bacterial products or the associated inflammation suppress pituitary LH secretion, and perturbspost partum ovarian follicular growth and function, which disrupts ovulation in cattle [5,12-14]. Thus, uterine disease is associated with lower conception rates, increased intervalsfrom calving to first service or conception, and more culls for failure to conceive [7,8,15,16].The goal of bovine reproduction management is to have cows become pregnant at a biologicallyoptimum time and at an economically profitable interval after calving. The timing ofexamination of animals after parturition should allow for the normal process of involution, yetalso provide time for treatment and response prior to the start of the breeding period. The aimsof uterine disease treatments are to reverse inflammatory changes that impair fertility, whilstenhancing the processes of uterine defence and repair.As bovine uterine disease is so important, it is not surprising that more than 500 papers havebeen published in the last 40 years on the most common uterine diseases, metritis, endometritisand pyometra [17]. Indeed, there are several review articles with extensive citation lists [1,18-23]. However, frequently the definition or characterization of the various manifestations ofuterine disease either lack precision or definitions vary between research groups and/or werenot validated as to their effect on reproductive performance, making assessment of the effectsof treatment difficult [24]. Often the term endometritis incorrectly includes metritis,endometritis and pyometra, and/or is determined solely on the basis of transrectal palpation ofan enlarged uterus [25,26]. During the 15th International Congress on Animal Reproduction(2004) it was suggested that the research field would be aided by clear definitions of uterinedisease that researchers could adopt. Thus, in the present paper we outline the key clinicalfeatures of uterine disease in cattle and suggest working definitions to reflect the character ofthese diseases.2. Uterine bacterial contamination and infectionThe majority of post partum inflammatory conditions of the uterus begin with bacterialcontamination of the uterine lumen. One should differentiate between uterinecontamination and uterine infection. The uterus of post partum cows is usually contaminatedwith a range of bacteria, but this is not consistently associated with clinical disease. Infectionimplies adherence of pathogenic organisms to the mucosa, colonization or penetration of theepithelium, and/or release of bacterial to xins that lead to establishment of uterine disease[27]. The development of uterine disease depends on the immune response of the cow, as wellas the species and number (load or challenge) of bacteria. The number of pathogenic bacteriain the uterus of post partum cows may be great enough to overwhelm uterine defensemechanisms and cause life-threatening infections, although these are relatively uncommon[1]. Indeed, it is non-life-threatening uterine infections that are most common and associatedwith impaired reproductive performance [8]. Furthermore, inflammation even in the absenceof active bacterial infection, may perturb embryo survival [28,29].Establishment of uterine bacterial infection may depend in part on the endocrine environmentand in particular progesterone seems to suppress uterine immune defences. Formation of thefirst post partum corpus luteum and secretion of progesterone precedes the onset of manyuterine infections [21,30]. Indeed, intrauterine infusions of Arcanobacterium pyogenes andEscherichia coli into post partum beef cows under experimental conditions did not establishinfections, unless peripheral plasma progesterone concentrations had started to increase [31].However, many spontaneous uterine infections are established within 3 wk of parturition,before ovulation of the first dominant follicle [5,32]. Furthermore, chronic uterine infectionand increased plasma concentrations of lipopolysaccharide (LPS) are associated withdisruption of the LH surge and failure of ovulation [1,14,33]. The relationship between uterinebacteria, the immune or inflammatory response, and ovarian function are complex and requiremore investigation, although it appears that uterine disease is associated with anovulatoryanestrus and cystic ovarian disease [12,34]. On the other hand, the immunosuppressive effectsof progesterone from the corpus luteum, or possibly adrenal steroids, may contribute to theprogression of uterine contamination into uterine infections. The mechanisms of action ofprogesterone are complex, not completely understood, and not within the scope of this article.However, the knowledge that progesterone is immunosuppressive at a number of levels and isinvolved in regulating the synthesis of prostaglandin F2α (PGF2α), plus a variety ofimmuomodulatory cytokines, can be useful for managing uterine infections. In cows with afunctional corpus luteum, administration of exogenous PGF2α is used to stimulate luteolysis,reduce progesterone and increase oestrogen concentrations, induce estrus and resolve uterineinfections [21,35,36]. Estrus appears to be particularly beneficial to the resolution of uterineinfection [37]. Exogenous PGF2α may enhance immune functions or increase uterine motilityto help the uterus resolve infections in animals that do not have active corpora lutea [38,39].However, the results of clinical trials of PGF2α for treatment of clinical endometritis in theabsence of an active corpus luteum are inconsistent [40-42]. Indeed, investigation by meta-analysis of many studies reporting the effect of prostaglandin F2 alpha administered postpartum indicated little benefit to the reproductive performance of dairy cattle [43]. Analternative effective treatment for endometritis is intrauterine infusion of antimicrobials [35,40,42].Involution of the genital tract after parturition also aids the resolution of uterine infection, andconversely may be delayed by uterine disease. In addition, evaluating uterine and cervicalinvolution may help to differentiate between physiological and pathological observations. Innormal cattle, the cervix re-opens after a week post partum [44]; and lochia is passed until 15to 20 d post partum and over the course of involution, lochia changes from a red-brown fluidto a more viscous yellow-white material. Healthy cows achieve a uterine horn diameter of 3to 4 cm by 25 to 30 d post partum, and cervical diameter < 5 cm by 40 d post partum, butcomplete involution of the uterus and cervix takes until approximately 40 to 50 d post partum[18,45]. However, uterine involution can also be affected by age, breed, nutrition and otherfactors so that delayed uterine involution is not a specific indicator of uterine disease [46].In summary, bacteria from the surface of the animal and the environment contaminate theuterine lumen of most post partum cows. Elimination of this contamination is dependent onuterine involution, regeneration of the endometrium, and uterine defense mechanisms. Theinflux of polymorphonuclear neutrophils (PMN), attracted by chemokines such as interlukin-8(IL-8), plays a key role in the uterine immune response [47]. However, ovarian activity andluteal progesterone modulate many of the processes that make a cow resistant or susceptibleto uterine infections, and exogenous PGF2α or intrauterine antimicrobials are effectivetreatments.3. PathologyTo the pathologist the general definitions of inflammation of the genital tract are simple.Inflammation limited to the endometrium is termed endometritis; involvement of the entirethickness of the uterine wall is metritis; of the serosa, perimetritis; and of the suspensoryligaments, parametritis [20,48]. Metritis can be distinguished from endometritis; in the former,all layers of the uterine wall show evidence of inflammation such as edema, infiltration byleukocytes, and myometrial degeneration. In both conditions, the mucosa is congested, andthere is a prominent leukocyte infiltration in response to the common pathogensArcanobacterium pyogenes, Fusobacterium necrophorum, Prevotella species and Escherichiacoli. In particular, infection with A. pyogenes is associated with increased time to pregnancy[16,49]. Endometritis is a superficial inflammation of the endometrium, extending no deeperthan the stratum spongiosum [20]; with histological evidence of inflammation (Fig 1(a) andFig 2(a)). During recovery from acute endometritis, there is fibrosis and leukocytosis, withdepletion of endometrial glands and atrophy of the remainder.Pyometra is associated with corpus luteum activity in the ovary, often its persistence for greaterthan the expected duration of the luteal phase. It has been suggested that it is the presence ofthis structure with its secretion of progesterone that results in endometritis developing intopyometra [48]. Early ovulation after parturition and formation of an active corpus luteum maypredispose to pyometra [50,51]. On the other hand, the retention of the corpus luteum may beassociated with failure of the luteolysin, prostaglandin F2α to reach the ovary. The role ofprogesterone may be to maintain functional closure of the cervix as well as increasing thesusceptibility to persistent infection, especially with A. pyogenes and anaerobic bacteria [51].4. Clinical definitionsPuerperal metritis is an acute systemic illness due to infection of the uterus with bacteria afterparturition. Puerperal metritis is characterized by the following clinical signs: a fetid red-brownwatery uterine discharge and, usually, pyrexia [52]; in severe cases, reduced milk yield,dullness, inappetance or anorexia, elevated heart rate, and apparent dehydration may also bepresent. The term metritis should be used for cows that have delayed involution and a fetiddischarge, in the absence of detected fever. Indeed, in some cases of severe bacterial infectionpyrexia was not detected even with daily monitoring of rectal temperature and did not dependon the load or species of bacteria [53]. Puerperal metritis is often associated with retainedplacenta, dystocia, stillbirth or twins and usually occurs toward the end of the first week postpartum, being rare after the second week post partum [52,54]. We propose that the definitionof clinical puerperal metritis in a cow should be characterized by overt systemic illness(decreased milk yield, dullness or other signs of toxaemia) associated with a fetid watery red-brown uterine discharge, often associated with fever > 39.5°C and an enlarged uterus. Animalsthat are not ill, but have an enlarged uterus and a purulent uterine discharge may be classifiedas having clinical metritis.Clinical endometritis is characterised by the presence of purulent (> 50% pus) ormucopurulent (approximately 50% pus, 50% mucus) uterine exudate in the vagina, 21 d ormore post partum, and is not accompanied by systemic signs [7,42]. Diagnostic criteria forclinical endometritis in post partum dairy cows, have been validated by examining factorsassociated with an increased time from parturition to conception [7]. The significant factorswere the presence of purulent vaginal mucus or a cervical diameter > 7.5 cm, 21 d or morepost partum; or, after 26 d post partum, the presence of a mucuopurulent material in the vagina.Using this classification for endometritis, the incidence was 16.9 % for the 1865 cowsexamined. The temporal differences in the significant factors probably reflect the progress ofuterine involution and immune defense. Classifying animals as having clinical endometritis ifthey are < 21 d post partum may include a greater proportion of animals that are spontaneouslyresolving bacterial contamination, and so reflect the presence of disease less accurately.Furthermore, variations in appearance of normal lochia confound diagnosis of endometritis atthis stage. Similarly, using delayed involution alone to diagnose endometritis is unreliable, asthe enlarged uterus may reflect physical damage or variations associated with breed, age, ornutrition rather than bacterial infection, whilst the small increase in diameter of the uterinehorns may be difficult to detect in mild cases of endometritis. Thus, although the pathology ofinterest involves the uterus, palpation of the uterus to asses its size lacks diagnostic accuracy[7,55]. However, estimation of cervical diameter by palpation was associated with clinicalendometritis and appears to be a more reliable marker of delayed involution [7,56,57]. Insummary, we propose that the definition of clinical endometritis in a cow is the presence ofpurulent uterine discharge detectable in the vagina 21 d or more post partum, or mucuopurulentdischarge detectable in the vagina after 26 d post partum.Subclinical endometritis can be defined as endometrial inflammation of the uterus usuallydetermined by cytology, in the absence of signs of clinical endometritis [58]. In animals withoutsigns of clinical endometritis, subclinical disease was diagnosed by measuring the proportionof neutrophils present in a sample collected by flushing the uterine lumen (Fig. 1(b) and Fig.2(b)), or using a cytobrush [19,59,60]. Subclinical endometritis was determined by the presenceof > 18 % neutrophils in uterine cytology samples collected 20 to 33 d post partum or > 10 %neutrophils at 34 to 47 d post partum, or by ultrasonic imaging of a small volume of mixedechogenicity fluid within the uterine lumen, in the absence of abnormal mucus in the vagina[60]. The incidence of clinical and subclinical endometritis was 53% at 40 to 60 d post partum,and was associated with delayed conception and increased culling [61]. The assessment ofinflammation at 40–60 days post partum corresponded approximately to >5% neutrophils[61]. Although investigation of subclinical endometritis is at an early stage, we have usedavailable data to suggest a working definition. We propose that a cow with subclinicalendometritis is defined by > 18 % neutrophils in uterine cytology samples collected 20 to 33d post partum, or > 10 % neutrophils at 34 to 47 d, or by ultrasonic imaging of mixedechogenicity fluid within the uterine lumen after 21 d post partum, in the absence of clinicalendometritis.Pyometra is characterized by the accumulation of purulent or mucopurulent material withinthe uterine lumen and distension of the uterus, in the presence of an active corpus luteum. Thereis often an increased number of pathogenic bacteria within the uterine lumen when the corpusluteum forms and pyometra occurs [51]. Although there is functional closure of the cervix, thelumen is not always completely occluded and some pus may discharge through the cervix intothe vaginal lumen. Pyometra is sonographically characterised by a corpus luteum in an ovary,accumulation of mixed echogenicity fluid in the uterine lumen and distension of the uterus. Insummary, we propose that pyometra is defined by the accumulation of purulent material withinthe uterine lumen in the presence of a corpus luteum and a closed cervix.5. DiagnosisIt is important to be able to diagnose the presence of uterine infection to facilitate timely andappropriate treatment and to quantify the severity of disease, which allows a prognosis to begiven for subsequent fertility. Unfortunately, there is no “gold standard” for diagnosis of uterinedisease, making it difficult to measure the sensitivity and specificity of clinical definitions. Inaddition, there is little information on the correlation between clinical and histopathologicalobservations, although the presence of pus in the vagina is correlated with the presence ofpathogenic bacteria in the uterus [62,63]. The definitions we propose should allowclassification of disease in most animals, whilst accepting that clinical parameters may notreflect the impact on economic or reproduction outcomes in all countries. Furthermore, thereis a continuum of peri-partum disease, so the consideration of what is abnormal and theselection of cost-effective therapy will depend on the production system. Therapeutic cut-points and decision trees would be useful for the different production systems.The diagnosis of puerperal metritis is made readily from the clinical signs of illness and fetiduterine discharge detectable on clinical examination. The diagnosis of pyometra depends ontransrectal palpation of a doughy, distended, thick walled uterus and/or transrectalultrasonography of mixed echogenicity fluid, and the presence of a corpus luteum. The uterine lumen fluid of a pyometra can be displaced from one horn to the other, which cannot be done with fluids associated with a gravid uterus. The sensitivity, specificity and positive predictive value of palpation for identifying mid-cyclic corpora lutea were 85%, 95.7% and 89.5%, respectively, whilst for ultrasonography the values were 95%, 100% and 100%, respectively [64]. If necessary, progesterone concentration in milk or plasma can be measured to avoid a small proportion of animals being misclassified by errors in the physical detection of a corpus luteum.The definitive diagnosis of endometritis is made on the basis of histological examination of endometrial biopsies (Fig. 1(a) and Fig. 2(a)), and these are predictive for subsequent fertility [49]. However, the technique is costly and time consuming, and not clinically accessible in most situations. Cytology is more practical (Fig. 1(b) and Fig. 2(b)) and is necessary to diagnose subclinical endometritis [58,60]. However, neither of these procedures produces a rapid clinical diagnosis. Thus, in the field, diagnosis of uterine disease usually relies on clinical examination. Transrectal palpation for delayed involution is not a good technique for evaluating uterine infection because it is subjective, uterine involution varies between cows, and there is little association with reproductive performance [7,21]. In addition, although a marked delay of uterine or cervical involution is associated with lower conception rates, it is the evaluation of animals where the effects on uterine involution are less obvious that is more difficult. Similarly, observation for abnormal vulval discharge is unreliable for diagnosis of endometritis [65]. The use of clinical records of stillbirth, twins, retained fetal membranes, dystocia and hypocalcemia helps identify animals at risk of uterine disease, but does not provide a specific diagnosis [54,65,66]. Further examination of data from a large clinical trial confirms that disease history alone lacks sensitivity for identifying cattle with clinical endometritis (Table 1). However, the use of historical information may decrease the cost of diagnosis and hence increase the cost : benefit of treatment for uterine disease for some farmers.The use of transrectal ultrasonography permits more objective measurement of the diameter of the uterine horns and cervix, and visualization of mucus and pus within the uterine lumen [11,60,67]. At present, there is little evidence that ultrasonography provides more information about clinical endometritis than examination of the contents of the vagina. Although, there is limited information on the relationship between ultrasonographic findings and clinical or subclinical endometritis, this is likely to be a fruitful area for research.To diagnose clinical endometritis we advocate the examination of the contents of the vagina for the presence of pus [7,22,42]. The simplest method is to perform a manual examination of the vagina and withdraw the mucus for inspection [68]. The advantage of this technique is that it is inexpensive, quick, provides additional sensory information such as detection of vaginal lacerations and detection of the odor of the mucus in the vagina. One procedure is to clean the vulva using a dry paper towel and insert a clean, lubricated gloved hand through the vulva into the vagina. The lateral, dorsal and ventral walls of the vagina and the external cervical os are palpated and the mucus contents of the vagina withdrawn for examination. The hand usually remains in the vagina for less than 30 seconds. Manual vaginal examination has been validated and does not cause uterine bacterial contamination, provoke an acute phase protein response, or delay uterine involution [68]. However, the operator has to be aware that vaginitis or cervicitis may give false results. Vaginoscopy can be performed using autoclavable plastic, metal or disposable foil-lined cardboard vaginoscopes, which allow inspection of the contents of the vagina. However, there may be some resistance to the use of vaginoscopes because of the perceived inconvenience, potential for disease transmission and cost [7]. A new device for examination of vaginal mucus (Metricheck®, Simcro, New Zealand) consists of a stainless steel rod with a rubber hemisphere that is used to rake out the vaginal contents.Several scoring systems have been described to estimate the severity of clinical endometritis[35,42,63]. The character of the vaginal mucus can be scored (Fig. 3) as well as odor (score 0for no odor and 3 for a fetid odor) [63]. The character score reflects the presence and semi-quantitative load of certain bacteria in the uterus. In one study [63], muco-purulent dischargewas associated with F. necrophorum and purulent discharge was associated withArcanobacterium pyogenes and Proteus species, whilst a fetid odor was associated with agreater load of Arcanobacterium pyogenes, Escherichia coli, Streptococci, and Mannheimiahaemolytica. Clear mucus with flecks of pus was not associated with the presence of highernumbers of pathogenic bacteria in the uterine lumen, but the effects on fertility are notconsistent [7,63]. These mild cases of endometritis may be resolving the uterine infection, andthe discriminators may not be sensitive enough to detect perturbation of reproduction.However, subclinical endometritis is associated with lower conception rates to first service andoverall [19,60]. Thus, the absence of pus in the vagina does not always reflect the absence ofinflammation in the uterus.6. ConclusionsIn conclusion, we have suggested clinical definitions for the common post partum uterinediseases that can be readily adopted by researchers and veterinarians. Given the diagnosticcriteria that we present, it is possible to identify individual cows that are likely to have ameaningful impairment of reproductive performance. A practical question is whether it iseconomically beneficial to invest the time and resources necessary to find and treat cows withendometritis. The optimum answer likely varies between farms, depending on the prevalenceof endometritis, the cost and accuracy of diagnosis, the efficacy and cost of treatment, thepressure for early post partum breeding, and the use of systematic breeding programs includingprostaglandin F2α for first insemination. Further research is needed to refine the inputs intoeconomic decision-making tools to answer these questions under a variety of managementconditions.AcknowledgementsSupported by The Wellcome Trust and BBSRC (to IMS), USDA Animal Health and Disease Funds (to ROG).We wish to thank the following people for kindly reviewing the manuscript, and contributing to this paper: AugustinePeter, Doug Hammon, Ram Kasimanickam, Marc Drillich, Wolfgang Heuweiser, John Mee, Pat Hartigan, Aart deKruif, Gyula Huszinicza, Hans Kindahl, Robert BonDurrant, Richard Murray and David Noakes.References1. Sheldon IM, Dobson H. Postpartum uterine health in cattle. Anim Reprod Sci 2004;82-83:295–306.[PubMed: 15271461]2. Elliot L, McMahon KJ, Gier HT, Marion GB. Uterus of the cow after parturition: bacterial content.Am J Vet Res 1968;29:77–81. [PubMed: 5688806]3. Griffin JFT, Hartigan PJ, Nunn WR. Non-specific uterine infection and bovine fertility. I. 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