**5. Postpartum metritis**

**3.8. Chronic degenerative endometritis**

**3.9. Persistent post-mating endometritis**

changes in the uterus [93].

274 Genital Infections and Infertility

post-breeding [100].

**4. Oophoritis and salpingitis**

gitis in mares results in sterility [103].

Chronic degenerative endometritis or endometriosis is degenerative change that occurs in older mares or following repeated inflammation of the uterus. Degenerative fibrosis can be the result of normal aging processes or may be the end-product of a life of continuous reinfection: anyway, healing uterine mucosa causes infertility in older mares [34]. Problems related to weaken reproductive structures can cause urinary retention, a condition in which the mares do not empty completely urine, especially during estrus. Thus, the retained liquid can cause inflammation and prevent conception. The use of antibiotics is not always good. One of the disadvantages of using antibiotics is the fact that kills good and bad bacteria, leaving the animal with no natural protection against future bacterial or fungal invasions. The definitive diagnosis can only be achieved by biopsy, which shows degenerative histological

Inflammation of the endometrium is caused by a response to exogenous materials introduced directly into the uterus at breeding, as components of the semen, extender in the case of AI, bacteria, and other debris [24, 96]. Two hormones, PGF2α and oxytocin, regulate myometrial contractions after the influx of neutrophils into the uterine lumen and their phagocytic activity after opsonization of the target [67]. This uterine defense mechanism reaches a pick at around 6–12 hours post-mating or AI [97]. In normal mares, most of the inflammatory products are cleared by physical uterine mechanisms within 48 hours after breeding, and the infection is cleared before the embryo leaves the fallopian tube and enters to the uterus on about days 5– 6 post-ovulation [98], the uterine inflammation has to be under control by 96 hours postovulation to maximize survival of the embryo [67]. A susceptible mare with persistent postmating endometritis is unable to clear such fluid by 96 hours, and the resulting prolonged inflammation generates an embryo-toxic environment. In addition, premature lysis of the CL is caused by PGF2α and subsequent progesterone deficiency, all contribute to embryo mortality and infertility [99]. This is more common in older and multiparous mares. They present with a history of short cycling and often and vaginal discharge approximately 2 weeks

After abdominal surgery or peritonitis, infectious inflammation of the ovaries (oophoritis) with abscessation and peritoneal adhesions may occur. Oophoritis could be a consequence of repeated transvaginal ultrasound-guided follicular aspiration [101, 102]. Affected mares present abdominal pain, anorexia, fever of unknown origin, and weight loss. Transrectal ultrasonography can help in the diagnosis of these infections. For the extend evaluation of the lesions and confirmation of the diagnosis, laparoscopy may be achieved. Ovariectomy is usually required for treatment of this condition [103]. Although it is rare in the mare, salpingitis may result from ascending infection of *Chlamydia* spp. as *Chlamidiaabortus* and *Chlamidia psittaci* after partum [74]. Salpingitis has been described in mares with CEM. Bilateral salpin‐ Postpartum uterine infections are of particular importance because of their severity and effect on the general health of the mare. The incidence of postpartum metritis—i.e., infection of the uterus within 7–10 days postpartum, sometimes involving the endometrium, myometrium, and perimetrium—in foaling mares is low but increases when birthing trauma and/or retained placenta occurs [2, 3]. Septic postpartum metritis is often a result of nonhygienic manipulation during foaling, obstetric manipulations, and retained placenta. Mares with postpartum may present severe systemic complications as endotoxemia and laminitis. The etiology of septic/ toxic metritis is associated with uterine atony or inertia. Trauma to the uterus, autolysis of placental remnants, and excessive lochia accumulation likely contribute to rapid growth of gram negative as *E. coli* and *K. pneumoniae* bacteria and production of toxins, which may be absorbed into the bloodstream, particularly when expulsion of contents is delayed or when the normally intact uterine mucosal barrier is damaged. Disruption of the endometrial mucosal barrier occurs during dystocia or gradually progresses after retention of fetal membranes leading to bacterial overgrowth and absorption of produced toxins. This process normally develops septic/toxic metritis and/or laminitis. Treatment consists of daily uterine flushers, systemic antimicrobial therapy, and therapy for endotoxemia. Laminitis and dehydration should be immediately initiated in affected mares [3, 104].
