Placentitis in mares is caused by bacteria ascending through the caudal genital tract and is a common reason of equine abortion in late gestation, and foal deaths in the first 24 h of their lives. The most commonly isolated pathogens associated with placentitis is Streptococcus equi subspecies zooepidemicus. The bacteria, which enter the pregnant uterus through the cervix, cause inflammation of the cervical star region of the placenta and subsequently travel along the umbilical cord and then they reach the amniotic fluid. Consequently foals swallow bacteria with amniotic fluid. Fetal infection is not always associated with premature births. Clinical signs connected with this conditions are premature udder development and presence of a vulvar discharge. However, precocious mammary gland development is also associated with twin pregnancies, and vulvar discharge is often difficult to detect without careful scrutiny. Diagnostic tools used to identify mares at risk of premature delivery mainly include transabdominal and transrectal ultrasonography of the pregnant uterus and the determination of maternal progestins concentration. Transrectal ultrasound examination of the caudal reproductive tract allows for direct examinations of the cervical star region, evaluation of fetal viability and evaluation of allantoic and amniotic fluids. The combined thickness of the uterus and placenta (CTUP) is also measured by transrectal ultrasonography. Normal values of CTUP are about 5 mm during midgestation and are less than 8 mm in month 10 of gestation, less than 10 mm in month 11 of gestation, less than 12 mm in month 12 of gestation - mares with placentitis have increased CTUP values. Generally mares with placentitis (chronic conditions) have increased concentrations of maternal progestins, sometimes for several weeks before abortion; however, in acute conditions progestins tend to decline hours or days before abortion. Treatment strategies for mares with ascending placentitis include combating infection, reducing inflammation and controlling myometral activity. The treatment should last from the onset of clinical signs until the delivery of the foal.
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