BACKGROUND Bovine besnoitiosis, caused by the apicomplexan parasite Besnoitia besnoiti, is a chronic and debilitating cattle disease that notably impairs fertility. Acutely infected bulls may develop respiratory signs and orchitis, and sterility has been reported in chronic infections. However, the pathogenesis of acute disease and its impact on reproductive function remain unknown. METHODS Herein, we studied the microscopic lesions as well as parasite presence and load in the testis (pampiniform plexus, testicular parenchyma and scrotal skin) of seven bulls with an acute B. besnoiti infection. Acute infection was confirmed by serological techniques (IgM seropositive results and IgG seronegative results) and subsequent parasite detection by PCR and histological techniques. RESULTS The most parasitized tissue was the scrotal skin. Moreover, the presence of tachyzoites, as shown by immunohistochemistry, was associated with vasculitis, and three bulls had already developed juvenile tissue cysts. In all animals, severe endothelial injury was evidenced by marked congestion, thrombosis, necrotizing vasculitis and angiogenesis, among others, in the pampiniform plexus, testicular parenchyma and scrotal skin. Vascular lesions coexisted with lesions characteristic of a chronic infection in the majority of bulls: hyperkeratosis, acanthosis and a marked diffuse fibroplasia in the dermis of the scrotum. An intense inflammatory infiltrate was also observed in the testicular parenchyma accompanied by different degrees of germline atrophy in the seminiferous tubules with the disappearance of various strata of germ cells in four bulls. CONCLUSIONS This study confirmed that severe acute besnoitiosis leads to early sterility that might be permanent, which is supported by the severe lesions observed. Consequently, we hypothesized that testicular degeneration might be a consequence of (i) thermoregulation failure induced by vascular lesions in pampiniform plexus and scrotal skin lesions; (ii) severe vascular wall injury induced by the inflammatory response in the testis; and (iii) blood-testis barrier damage and alteration of spermatogenesis by immunoresponse.

中文翻译：

---

血管壁损伤和炎症是造成公牛急性贝氏病早期睾丸变性的关键病原机制。

背景技术由apiplexplexan寄生虫Besnoitia besnoiti引起的牛良性病是一种慢性且使人衰弱的牛疾病，特别损害了生育能力。急性感染的公牛可能会出现呼吸道症状和睾丸炎，据报道在慢性感染中不育。然而，急性疾病的发病机理及其对生殖功能的影响仍然未知。方法在本文中，我们研究了7例急性贝氏芽孢杆菌感染公牛的睾丸（皮膜状丛，睾丸实质和阴囊皮肤）的微观病变以及寄生虫的存在和负荷。通过血清学技术（IgM血清学阳性结果和IgG血清学阴性结果）以及随后通过PCR和组织学技术进行的寄生虫检测证实了急性感染。结果最被寄生的组织是阴囊皮肤。此外，如免疫组织化学所示，速殖子的存在与脉管炎有关，三头公牛已经形成了幼年组织的囊肿。在所有动物中，绒毛状丛，睾丸实质和阴囊皮肤均出现明显的充血，血栓形成，坏死性血管炎和血管生成等现象，证明严重的内皮损伤。在大多数公牛中，血管性病变与慢性感染特征性病变并存：角化过度，棘皮症和阴囊真皮中明显的弥漫性纤维化。在睾丸薄壁组织中还观察到强烈的炎症浸润，伴有生精小管中不同程度的生殖细胞萎缩，四头公牛的生殖细胞各层消失。结论这项研究证实严重的急性贝氏病可导致早期的不育，这种不育可能是永久性的，这被观察到的严重病变所支持。因此，我们假设睾丸退化可能是由于（i）脂膜状丛和阴囊皮肤病变中的血管病变引起的温度调节衰竭；（ii）睾丸炎性反应引起的严重血管壁损伤；（iii）血液睾丸屏障损伤和免疫反应引起的精子发生改变。（ii）睾丸炎性反应引起的严重血管壁损伤；（iii）血液睾丸屏障损伤和免疫反应引起的精子发生改变。（ii）睾丸炎性反应引起的严重血管壁损伤；（iii）血液睾丸屏障损伤和免疫反应引起的精子发生改变。