Placentitis in mares emerged as a leading cause of reproductive loss in the equine breeding industry, with considerable economic impact when a pregnancy ends in abortion or the birth of a small, ill-thrift foal. Learn about what causes placentitis in mares, how to diagnose and treat it, and better understand the anticipated outcome of this condition.
What causes placentitis in mares?
Although there are multiple causes of equine placentitis, it is seen commonly in the mare due to an ascending infection of bacteria through the cervix. Organisms enter the chorioallantois (the “placenta”), colonize the cervical star region, produce pro-inflammatory cytokines, and release prostaglandins that contribute to the cascade of events leading to premature delivery of a preterm foal. The common pathogens are Streptococcus equi zooepidemicus, Klebsiella pneumonia, Escherichia coli, Pseudomonas aeruginosa, and Staphylococcus species. Placental pathology at the cervical star (the avillous portion of the placenta abutting the cervix) is often observed. History and clinical signs usually involve premature udder development and/or premature lactation (this should happen a couple of weeks before parturition, not months before) with or without vulvar discharge. A reproductive examination should include a transabdominal ultrasound for fetal viability, vaginal exam with a speculum to inspect the cervix and look for discharge, and a transrectal ultrasound to measure the combined thickness of the uterus and placenta (CTUP).
How to diagnose and treat ascending placentitis in mares
The CTUP is dynamic and accurate measurements must be made just cranial to the cervix between the middle uterine artery and allantoic space (Figure 1). An average of at least three CTUP measurements should be calculated and there are several points to consider that will alter the accuracy. Physiological edema occurs dorsally and thus measurements should be taken ventrally. The active foal abutting the cervix will also alter the CTUP measurements and thus should be taken when the foal is quiet. At this time, the echogenicity of the fetal fluids should be noted as well as any evidence of placental separation.
Treatment goals include inhibiting/eliminating bacterial growth, maintaining uterine quiescence, decreasing uterine contractions, increasing cervical tone, and increasing blood supply to uterus and placenta whilst counteracting endotoxemia. Treatment is a multidrug approach. Antimicrobials are a mainstay therapy, usually broad spectrum as samples for culture and susceptibility are not always feasible to obtain. These include potassium penicillin (22,000 IU/kg IV QID) and gentamicin (6.6 mg/kg IV SID) or trimethoprim sulfa (30 mg/kg PO BID) because they accumulate in the allantoic fluid. Progestogens in the form of altrenogest (Regumate; 0.088 mg/kg PO q24 hr) are administered throughout or gradually decreased close to foaling depending on the clinician. Mares will foal despite progesterone treatment. Anti-inflammatory agents are necessary as bacteria/products stimulate cell-mediated immune mechanisms and release of inflammatory cytokines that promote uterine contractions. Flunixin meglumine (1 mg/kg PO or IV BID; 0.25 mg/kg PO or IV QID), phenylbutazone, and firocoxib (selective Cox2 inhibitor) have been used. Pentoxifylline can be added as well. It is a phosphodiesterase inhibitor and free-radical scavenger that helps promote blood flow to the placenta due to rheologic properties. True tocolytics, such as clenbuterol, may be administered but may have limited use in horses for preventing myometrial contractions.
Other forms of equine placentitis
Other placentitis causes of abortion include fungal, nocardioform, and leptospirosis. The main causative agents of fungal abortion include Aspergillus and Candida. Several etiologic agents have been associated with nocardioform abortion, including Crossiella equi (gram+, non-acid fast, filamentous branching) and Amycolatopsis sp. (gram+). These occur commonly in central Kentucky. There is no age or breed predilection and it is not associated with management. Mares abort in late gestation or prematurely deliver stillborn/weak foals. Placentitis can be diagnosed prior to abortion by transabdominal ultrasound of hyperechoic fluid at the base of the lowest area of the uterus (Figure 2), but lesions can often be difficult to image.
Characteristic placental lesions are seen at the junction of the uterine body and base of the gravid uterine horn (Figure 3). The chorionic surface is brown, sticky, mucoid, and dotted with white granular structures and can mimic mycotic (“fungal”) placentitis.
Treatment is similar to that of ascending placentitis, albeit unrewarding. Mares clear the infection spontaneously following abortion and can be bred back normally without increased risk for repeat infection. Recently, it was described that nocardioform placentitis cases in Kentucky decrease with rainfall and increase with ambient temperatures. Thus, nocardioform species are likely infecting mares from an environmental source; however, attempts to induce nocardioform placentitis experimentally have been unrewarding.
Leptospirosis abortion is commonly caused by the following serovars and is zoonotic: L. grippotyphosa, L. pomona (most common serotype causing abortion), and L. bratislava. Horses can serve as reservoir hosts with persistent shedding in urine. Transmission involves contact with environmental infection (infected urine, aborted fetuses, contaminated feed or water) and the organism reaches the fetus via hematogenous spread. Clinical signs may include fever, anorexia, jaundice; abortion occurs one to three weeks after clinical signs. Diagnosis is made by detection of maternal antibodies, spirochetes found in fetal kidney, placenta, or maternal urine, and/or a characteristic placental lesion: cystic nodular (adenomatous) allantoic hyperplasia. Treatment involves antimicrobial therapy with procaine penicillin G or oxytetracycline, which may not eliminate shedding but may prevent fetal infection. Leptospirosis abortion prevention includes keeping horses fenced away from swampy areas with stagnant water or run-off water from other animals (cattle, pigs, dogs, wildlife) and isolation of shedders. Horses can shed organisms for up to three months and therefore three negative fluorescent antibody tests are recommended. An FDA-approved vaccine is also available for protection against L. pomona.
Future research
Even on well-managed Thoroughbred farms the incidence of placentitis-induced abortion can be up to five percent. Management of the high-risk pregnant mare is labor intensive and costly. Therefore, predictors to accurately diagnose equine placentitis and monitor treatment response would be of significant value. To date, experimental models of equine ascending placentitis have been used to demonstrate a significant rise in maternal serum amyloid A (SAA) levels after transcervical bacterial inoculation of the placenta. SAA is an acute phase protein produced by the liver as a result of infectious and/or inflammatory responses that can be detected in the blood. Data demonstrating SAA as a novel biomarker of equine ascending placentitis holds much promise. However, experimental models do not always accurately mimic clinical disease. We know that healthy pregnant mares have low levels of SAA the last four months of gestation, then demonstrate a rise in SAA at the time of foaling and return to baseline by one month postpartum. Establishing the response of SAA in spontaneously occurring cases of placentitis can enhance the veterinarian’s ability to evaluate specific antimicrobial efficacy as well as the efficacy of tocolytics and anti-inflammatory medications.