Introduction:
Placental pathology represents the most common cause of preterm delivery, fetal death, stillbirth and neonatal disease worldwide (Whitwell 1980). Placentitis refers to inflammation of the chorioallantois, usually caused or complicated by infective agents and frequently extending to the amnion and the umbilical cord (funisitis). The inflammatory response may vary in intensity from slight to severe and show a variable distribution from localised to diffuse. In general, the location of placentitis reflects the route by which the infection entered the uterus. A large number of infective agents have been implicated, many being opportunistic or environmental invaders (Whitwell 1988). Viral, bacterial, fungal and protozoal agents have being identified as causative agents of placentitis. Annual variations in numbers and types of placentitis reported in different geographical areas suggest the possible role of environmental factors in the incidence of the condition (i.e. MRLS in Kentucky 2001 - 2002).

Lesions distribution:

Ascending placentitis:
Placentitis in mares is reported to be most commonly caused by microrganisms ascending through the vagina and breaching the cervical barrier. An active role of the cervix in the pathogenesis of the condition is therefore implicit. If there are bacteria and/or fungi on the cervix and the cervical seal is compromised, they can enter the uterus and cause placentitis. Anatomical, hormonal or even neurological factors contributing to cervical incompetence and/or increased perineal or vaginal contamination will increase the risk of ascending placentits. Cervical inefficiency due to critical cervical shortening in mid gestation has been extensively described in women as a leading cause of preterm delivery, with no convincing evidence as to the possible cause. Progesterone administration and cervical cerclage have been used as effective means to correct the condition in the absence of infection (Vidaeff and Ramin 2009). A similar condition has been observed in pregnant mares in recent years and a similar therapeutic approach appears to be highly beneficial. Cervical placentitis tends to recur in some mares and preventive strategies should be implemented, including ultrasound (US) monitoring of the cervix and cervical pole CTUP from mid gestation to term.
Ascending placentitis generally develops and progresses slowly during the course of weeks or months before clinical signs become apparent. The more chronic the infection the more extensive or pronounced the lesions of chorionic thickening and fetal growth restriction are likely to be. Depletion of chorionic villi, thickening, discoloration are commonly observed at the cervical pole of the affected placenta, often associated with a fibro-necrotic exudates. Thickening at the cervical star can prevent it rupturing at birth or abortion, so that the chorion tears across the rostral body. In about
12% of cases, infection will rapidly spread to the fetus causing septsis and abortion, before placentitis has become grossly evident. A variety of bacteria can be associated with ascending placentitis, but most commonly Streptococcus sp. and E. Coli.

Diagnosis:
Diagnosis of placentitis during gestation is often difficult as most mares show no outward signs of infection. Some mares will show signs of premature mammary development and lactation, cervical softening and occasionally a vaginal discharge. Transrectal and transabdominal ultrasound examinations are very useful in diagnosing placentitis and assessing fetal viability. Ultrasound features of a diseased placenta include diffuse echolucency (oedema), increased CTUP (>15 mm at term) (Renaudin et al.
1997), loss of contact between uterus and chorioallantois, accumulation of fluid and/or echogenic material, cervical relaxation (prior to 9 months gestation) (Bucca and Fogarty 2011). After delivery/birth gross examination and histopathology of fetal membranes will confirm US diagnosis.
Placentitis results in several outcomes. In addition to abortion, stillbirth and pre-term birth, the mare may produce small weak foals, small normal and normal foals. Small, weak neonates represent a special management and medical challenge, as they carry an increased risk of developing sepsis and orthopaedic problems and suffer a degree of prematurity. Small normal neonates usually result from mares displaying clinical signs for quite sometimes. These foals usually do well, as they have completed their fetal maturation stage in preparation of birth. They still carry a risk for sepsis and orthopaedic complications.

Treatment:
Treatment of placentitis is often unrewarding, when the mare has developed clinical signs. Treatment aims at maintaining gestation for as long as possible to enhance neonatal viability, due to our limited ability at handling premature neonates. Every effort should be made to limit further infectious spread, reduce the inflammatory response and reduce the risk of increased myometrial contractility in response to inflammation. Experimental models examining the relationship between pro-inflammatory cytokines and placentitis showed that bacterial infection causes increased expression of pro-inflammatory cytokines leading to the release of PGE2 and PGF2alpha into the allantoic fluid and premature labour (LeBlanc et al. 2002). Lyle et al. (2009) elegantly showed that the fetal hypothalamic-pituitary-adrenal axis is activated subsequent to infection or inflammation. Evidence suggesting that the synthesis of PGE2 and PGF2alpha is driven by cytokines in concert with fetal cortisol indicate that treatment strategies that fail to interrupt the inflammatory cascade and reduce fetal stress may be ineffective in preventing pre-term delivery.