LeBlanc M M, Causey R C
Rood and Riddle Equine Hospital, Lexington, KY 40580, USA.
Reprod Domest Anim. 2009 Sep;44 Suppl 3:10-22. doi: 10.1111/j.1439-0531.2009.01485.x.
Endometritis, a major cause of mare infertility arising from failure to remove bacteria, spermatozoa and inflammatory exudate post-breeding, is often undiagnosed. Defects in genital anatomy, myometrial contractions, lymphatic drainage, mucociliary clearance, cervical function, plus vascular degeneration and inflamm-ageing underlie susceptibility to endometritis. Diagnosis is made through detecting uterine fluid, vaginitis, vaginal discharge, short inter-oestrous intervals, inflammatory uterine cytology and positive uterine culture. However, these signs may be absent in subclinical cases. Hypersecretion of an irritating, watery, neutrophilic exudate underlies classic, easy-to-detect streptococcal endometritis. In contrast, biofilm production, tenacious exudate and focal infection may characterize subclinical endometritis, commonly caused by Gram-negative organisms, fungi and staphylococci. Signs of subclinical endometritis include excessive oedema post-mating and a white line between endometrial folds on ultrasound. In addition, cultures of uterine biopsy tissue or of small volume uterine lavage are twice as sensitive as guarded swabs in detecting Gram-negative organisms, while uterine cytology is twice as sensitive as culture in detecting endometritis. Uterine biopsy may detect deep inflammatory and degenerative changes, such as disruption of the elastic fibres of uterine vessels (elastosis), while endoscopy reveals focal lesions invisible on ultrasound. Mares with subclinical endometritis require careful monitoring by ultrasound post-breeding. Treatments that may be added to traditional therapies, such as post-breeding uterine lavage, oxytocin and intrauterine antibiotics, include lavage 1-h before mating, carbetocin, cloprostenol, cervical dilators, systemic antibiotics, intrauterine chelators (EDTA-Tris), mucolytics (DMSO, kerosene, N-acetylcysteine), corticosteroids (prednisolone, dexamethasone) and immunomodulators (cell wall extracts of Mycobacterium phlei and Propionibacterium acnes).
子宫内膜炎是母马不育的主要原因,源于配种后细菌、精子和炎性渗出物未能清除,通常难以诊断。生殖器官解剖结构缺陷、子宫肌层收缩、淋巴引流、黏液纤毛清除、宫颈功能,以及血管退化和炎症衰老等因素导致母马易患子宫内膜炎。诊断通过检测子宫积液、阴道炎、阴道分泌物、发情间期缩短、炎性子宫细胞学检查及子宫培养阳性来进行。然而,亚临床病例可能没有这些症状。刺激性水样中性粒细胞渗出物分泌过多是典型的、易于检测的链球菌性子宫内膜炎的特征。相比之下,生物膜形成、黏稠渗出物和局部感染可能是亚临床子宫内膜炎的特征,通常由革兰氏阴性菌、真菌和葡萄球菌引起。亚临床子宫内膜炎的症状包括配种后水肿过度以及超声检查时子宫内膜褶皱间出现白线。此外,子宫活检组织培养或小容量子宫灌洗在检测革兰氏阴性菌方面的敏感性是保护拭子的两倍,而子宫细胞学检查在检测子宫内膜炎方面的敏感性是培养的两倍。子宫活检可检测到深层炎症和退行性变化,如子宫血管弹性纤维破坏(弹性组织变性),而内窥镜检查可发现超声检查看不到的局部病变。患有亚临床子宫内膜炎的母马配种后需要通过超声进行仔细监测。可添加到传统疗法(如配种后子宫灌洗、催产素和子宫内抗生素)中的治疗方法包括配种前1小时灌洗、卡贝缩宫素、氯前列醇、宫颈扩张器、全身用抗生素、子宫内螯合剂(乙二胺四乙酸 - 三羟甲基氨基甲烷)、黏液溶解剂(二甲亚砜、煤油、N - 乙酰半胱氨酸)、皮质类固醇(泼尼松龙、地塞米松)和免疫调节剂(草分枝杆菌和痤疮丙酸杆菌细胞壁提取物)。