IN-DEPTH INTERACTIVE: REPRODUCTIVE DISORDERS – PATHOLOGY TO TREATMENT


drome.64 The pathophysiology of this condition is poorly understood. Information from a well-established model of pla- centitis has provided a better understanding of the disease process.65–69 Placental infection usually occurs in the last trimester of gestation. In most cases, bacteria invade the caudal reproductive tract and migrate through the cervix to the placenta. Infective organisms colonize the caudal placenta at the cervical star and disrupt the intimate contact between the allantochorion and endometrium. In- fection induces an inflammatory cascade with the production of cytokines and prostaglandins. Mares with induced placentitis showed higher interleukin 6 and 8 concentrations in their placentas, elevated


concentrations of prostaglandins E2 and F2 in al- lantoic fluid, and increased duration and intensity of uterine contractions compared with uninfected, con- trol mares. Resultant uterine contractions cause premature fetal expulsion. Premature delivery usually precedes fetal exposure to cortisol and mat- urational processes essential for survival. How- ever, in some cases, inflammation activates the hypothalamic pituitary axis, stimulates cortisol re- lease, and induces maturation of the lungs and gut prior to delivery, thus improving foal survival. Histopathologic findings from the placentitis


model revealed bacteria on the chorionic surface, allantoic and umbilical inflammation, and bacterial colonization in fetal lungs.69 It is postulated that fetal infection occurs when bacteria passes through fetal membranes and into amniotic fluid that the fetus inhales or swallows. Not all fetuses become infected with placentitis. This scenario is particu- larly true in mares infected with nocardia-type or- ganisms (actinomycete bacteria such as C. equi and Amycolatopsis spp.), in which there is significant infection and inflammation in the placental tissues but not the fetus.


Diagnostic Tools for Differentiating Mares With Placentitis


Clinical Signs The most common clinical signs of placentitis in- clude premature udder development and purulent vulvar discharge. Vulvar discharge is often the first sign of infection but is frequently undetected if the mare’s perineal region is not monitored daily.70 Premature mammary gland development can occur in mares with twin pregnancies as well as in mares with placentitis, likely as a secondary response to activation of the hypothalamic pituitary axis. His- torical information regarding breeding and identifi- cation of mares with twins helps differentiate these mares from mares with placentitis. It is notewor- thy that some mares have scant to no vulvar dis- charge present and/or minimal udder development but have fulminant placental infection. These mares may suffer a subclinical infection that results in death of the fetus. Alternatively, some mares have extensive placental separation as a result of


Table 2. Normal Values for Ultrasound Measurement of CTUP Gestational Day 271–300


CTUP (mm) 8


301–330 330


10 2


CTUP, combined thickness of the uterus and placenta.


infection but will deliver viable foals. Mares af- fected with nocardia-form placentitis often have sig- nificant placental compromise at the juncture of the uterine body and pregnant uterine horn and produce copious purulent material. Surprisingly, the fetus is not infected. The inflammation present in nocar- dia-form placentitis induces hypothalamic-pituitary activation, which promotes cortisol release and pre- cocious maturation of the foal. These events can improve foal survival even in the face of early delivery. Systemic health is rarely compromised in mares


with placentitis. Blood counts, serum chemistry values, and blood lactate usually fall within normal ranges. Mares will rarely develop a systemic ill- ness similar to metritis when affected with placental infections.


Transrectal Palpation and Ultrasonographic Examination


Transrectal ultrasonography in late gestation is a useful tool for evaluating placental integrity (at the cervical star), fetal activity, and fetal fluid charac- ter.71 Fetal orbit diameter can be measured to es- timate fetal age. The diagnosis of late gestational twins is not reliable from a transrectal ultrasono- graphic examination. The caudal aspect of the allantochorion at the cervical star is the most frequently affected area in mares with placentitis because of the ascending route of infection. Thoroughly examining this area using transrectal ultrasonography is critical when diagnosing placentitis. In normal pregnant mares, the combined uterine and placental (chorioallantoic) unit is measured. Values of the combined thick- ness of the uterus and placenta (CTUP) for mares with normal pregnancies have been established (Table 2).71 Mares with placental infection or in- flammation will have an increase in CTUP measures or separation of the membranes with the presence of purulent material.72 A 5- or 7.5-MHz linear trans- ducer is placed in the rectum and positioned 5 cm cranial to the cervical-placental junction. The trans- ducer is moved laterally until the large uterine vessel is visible at the ventral aspect of the uterine body. The CTUP is measured between the uterine vessel and allantoic fluid. Aminimum of 3 measures should be obtained and averaged. Along with clinical signs, this tool is often the first line of defense for detecting placentitis. In one study,73 serial transrectal ultra- sound examinations were performed in mares that


AAEP PROCEEDINGS  Vol. 61  2015 285


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