Placentitis in the Mare - Causes, Diagnosis and Treatment

April 02, 2014

Placentitis, an inflammation of the placenta usually caused by an infectious agent, has emerged as a leading cause of reproductive loss in the equine breeding industry. This has a large economic and emotional impact when the pregnancy progresses until close to term but unfortunately ends in abortion or the birth of a small ill-thrifty foal. The placenta is composed of the amnion, which surrounds the fetus and the chorioallantois that attach to the endometrium of the mare. These structures protect the fetus and provide gas and nutrient exchange allowing the foal to grow. When placentitis occurs it usually affects the chorioallantois compromising the foal because there is a loss of attachment of the placenta to the endometrium or the presence of infection and inflammation.  In this article, Dr. Karen Wolfsdorf of the Hagyard Equine Medical Institute, discusses the causes, diagnosis and treatment of placentitis in the mare.


Placentitis is most commonly caused by bacteria. These organisms gain access to the placenta and potentially the fetus by three characteristic mechanisms.

Placentitis_Fig 1Ascending infection: This occurs when the pathogen gets past the vulva lips and the vestibulo-vaginal sphincter (hymen) and enters the cervix. The bacteria proceed to destroy the microvilli preventing gas and nutrient exchange in that area. The lesion and bacteria spread from the cervical star region moving cranially to the body of the uterus and towards the fetus. A clear line of demarcation can be seen where the avillus and villus areas meet (photo left; ascending placentitis originating at the cervical star). Abortion is due to fetal death from septicemia, placental insufficiency (lack of nutrients and gas exchange) or the inflammatory process causing the uterus to contract. The most common pathogens in ascending placentitis include Streptococcus spp, Escherichia coli, Pseudomonas spp., Klebsiella spp., Staphylococcus spp, and the fungus Aspergillus. Differentiation between bacterial and fungal lesions is not possible by visual observation of the placenta.

Hematogenous infection: This occurs when a mare is systemically sick or bacteremic and the organism seeds within the vasculature of the uterus/ placenta and fetus. Leptospirosis spp., Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus, Streptococcus and Salmonella abortus equi are bacteria that can enter by this mechanism.

Placentitis_Fig 3 The last means is unidentified and has been attributed to a gram-positive branching bacillus and described as a mucoid or Nocardioform placentitis. Crossiella equi spp., and Amycolatopsis spp., are the two most common organisms identified to produce the characteristic lesions. They produce an extensive and severe exudative placentitis focused at the most dependent part of the uterus, at the placental body and horns rather than at the cervical star (photo right; nocardioform placentitis with mucoid exudate and avillus area at the bifurcation of the uterus). This sticky brown mucous lies above a well-defined avillus area of the placenta. Cultures taken of these slow growing bacteria should be held for at least 72 hours to provide sufficient time for growth. Unfortunately, how these organisms gain access to the uterus and placenta is not known. One theory is that they enter the uterus when the mare is in estrus possibly at the time of breeding. However, a questionnaire launched by The University of Kentucky Gluck Equine Center, to affected farms during the 1999 breeding season revealed that no predisposing factors could be identified. Studies by University of Kentucky Gluck Equine Center in which Nocardioform bacteria were given orally, intravenously, intranasally and intrauterine were unable to duplicate the disease. Therefore, further research is needed to elucidate this mechanism.


Placentitis_Fig 4Clinical signs of placentitis include vaginal discharge and premature lactation. Ascending infections may show one or both of these signs where as hematogenous and mucoid usually only show premature lactation. A diagnosis usually can be determined using trans-rectal and/or trans-abdominal ultrasound in combination with a culture if a vaginal discharge is present. The culture can identify the infective organism and provide antibiotic sensitivity to help with treatment. Measurements of maternal progestagens and total estrogen can help corroborate the placental and fetal well-being.

Trans-rectal ultrasonographic evaluation of the caudal reproductive tract has become a routine diagnostic tool for placentitis. Renaudin and co-workers developed the technique for evaluation of the combined thickness of the uterus and placenta (CUPT) and established normal values in mares throughout gestation. Consistent measurements can be taken one to two centimeters cranial ventral to the cervical star (photo left; measurement of the combined uteroplacental thickness (CUPT) at cervical star using transrectal ultrasonography). Since ascending infections are most common and initiated at the cervical star, ultrasonographic examination of this area is warranted.

Placentitis_Fig 5 Transabdominal ultrasonography is an extremely useful aid in evaluating fetal viability and placental abnormalities. Although placental thickening is difficult to consistently interpret trans-abdominally due to the stretching and contracture of the different regions of the pregnant uterus, separation of the chorioallantois from the endometrium and the presence of exudate as seen with mucoid or hematogenous placentitis may be identified (photo right; trans abdominal ultrasound revealing separation of the placenta from the uterus with exudate between). Volume and echogenecity of the fetal fluids can be evaluated as well as fetal heart rate, tone, activity and size.


For pregnancy to be maintained the fetus needs to develop in a quiet environment, free of infection and inflammation with the placenta providing adequate blood flow for nutrition and gas exchange. Although bacterial infection initiates disease, based on recent work from an experimental model of ascending placentitis in pony mares, premature delivery may occur secondary to inflammation of the chorion rather than as a consequence of fetal infection. With Nocardioform placentitis it appears, however that the placental separation/disruption due to the mucoid exudate causes placental insufficiency leading to fetal compromise. Therefore, therapies are directed at resolving microbial invasion, decreasing inflammation and uterine contractions. Systemic treatment can include antibiotics, exogenous progestagens, anti-inflammatories, tocolytic agents (decrease uterine contraction) and medications that improve uterine perfusion.

In mares that are considered high risk (those that have a history of previous feto-placental compromise, cervical incompetency/lacerations, chronic disease, old age, poor reproductive conformation), routine placental ultrasonographic evaluations, in conjunction with fetal viability assessments and serial hormonal evaluations, allow early determination of placental and fetal problems. These preventative measures in combination enable identification and treatment of a problem early in the course of infection, providing the opportunity for the birth of a healthier foal. Unfortunately, therapeutic protocols are still mostly derived from extrapolation from human literature, non-pregnant mare research and clinical impressions. Future studies will hopefully identify markers of infection and inflammation characteristic for placentitis so treatment can be initiated early.