Also see Horses.
The most common noninfectious cause of abortion in horses is twinning. Most abortions related to twinning occur at 8–9 mo of gestation and may be preceded by premature lactation. Placental insufficiency ultimately causes abortion of twins. Umbilical cord abnormalities, such as torsion due to abnormal length (>100 cm), have been incriminated in abortions. Diagnosis of abortion due to cord torsion requires evidence of localized swelling or hemorrhage because torsions occur in some normal births. Signs of fetal circulatory disturbances, such as subcutaneous edema, a swollen, soft liver, and microscopic mineralization of placental vessels, are also signs of umbilical cord obstruction. Ectopic pregnancy is rare but may result in abortion at 7–10 mo of gestation.
Mare Reproductive Loss Syndrome
In the spring of 2001, horse farms in Kentucky and neighboring states experienced an explosive outbreak of early abortions and late-term abortions, stillbirths, and weak foals that died within a few days. Simultaneously there was a large increase in fibrinous pericarditis and unilateral uveitis in horses of all ages and both sexes. Together these conditions became known as mare reproductive loss syndrome (MRLS). Analysis of records showed that MRLS had occurred in the area in earlier years. MRLS has since been diagnosed in states as far away as New York and Florida. An abortion storm with similar clinical signs and risk factors was recently reported from Australia.
The majority of early abortions occur at 40–80 days of gestation, with some losses occurring as late as 140 days. A few affected mares have colic, fever, and/or purulent vulvar discharge, but the majority remain clinically normal. Typically the first sign is abortion or finding a fetus dead in utero by ultrasound. Most fetuses are expelled within 2 days to 2 wk of dying and are autolytic. Neutrophilic placentitis and metritis are usually present. Most mares rebred during the same breeding season do not become pregnant, but conception is usually normal during the next breeding season. Late term losses generally occur at 10 mo of gestation to term, and the mare usually does not display signs of impending parturition. The placenta and umbilical cord are thickened, edematous, and discolored light brown to yellow. Neutrophilic inflammation of the umbilical cord and placenta are usually present, with the neutrophilic funisitis being characteristic of the syndrome. A variety of bacteria can be isolated from the fetuses, regardless of when they abort, but are not considered causative. Pasture exposure to eastern tent caterpillars (Malacosoma americanum) is an important risk factor, and both early and late-term abortions have been reproduced by oral administration of whole caterpillars or their exoskeletons, but not their digestive tract. The mechanism causing abortion has not been confirmed. It has been proposed that an unidentified toxin associated with the exoskeleton of these caterpillars is involved, and that bacterial infections are secondary. Alternatively, caterpillar hairs may penetrate the oral or intestinal mucosa and carry bacteria, resulting in bacteremia with localization in the uterus and other organs. (The horses in the Australian outbreak were exposed to processionary caterpillars [Ochragaster lunifer]).
Prevention consists of pasture management to control the numbers of eastern tent caterpillars and other procedures to prevent exposure of pregnant mares to eastern tent caterpillars.
Fescue Grass Toxicosis
Ingestion of fescue infected by the endophyte Acremonium causes prolonged gestation, agalactia, edema and premature separation of the placenta, and perinatal death. The placenta is thickened and edematous and does not rupture normally at the cervical star. The chorioallantois precedes the foal through the birth canal instead of remaining attached to the uterus, resulting in anoxia and death of the fetus. The source of the infected fescue can be pasture, hay, or bedding. (See also Fescue Poisoning.)
Infectious causes of abortion include viral diseases (such as equine rhinopneumonitis and equine viral arteritis) as well as bacterial and fungal infections.
Equine Rhinopneumonitis (Equine Herpesvirus 1 Infection)
This is the most important viral cause of abortion in horses. Abortion is usually after 7 mo of gestation and is not preceded by maternal illness. The placenta may be edematous or normal. Gross fetal lesions include subcutaneous edema, jaundice, increased volume of thoracic fluid, and an enlarged liver with yellow-white lesions ∼1 mm in diameter. Histologically, these lesions represent areas of necrosis containing intranuclear inclusions. Inclusion bodies are also found in necrotic lymphoid tissues. There is often a necrotizing bronchiolitis. Diagnosis is by fluorescent antibody, PCR, or virus isolation from fetal tissues. Prevention is based on vaccinating at 5, 7, and 9 mo of gestation as well as preventing exposure of pregnant mares to horses attending shows or other equine events. (See also Equine Herpesvirus Infection.)
Equine Viral Arteritis (EVA)
Abortion may follow clinical cases of EVA by 6–29 days. Arteritis may be found in the fetal myocardium or placenta, but usually there are no fetal lesions. Stallions can be persistently infected, and EVA can spread venereally or by aerosol. Diagnosis is by a history of EVA shortly before abortion, virus isolation or PCR of placenta and/or fetal tissues, or by seroconversion of the dam. Prevention of EVA is by management to minimize viral transmission in breeding populations and to prevent development of carrier stallions. In the USA, a licensed modified live virus vaccine is available for use in nonpregnant mares. Antibody titers resulting from vaccination and natural infection cannot be differentiated, and the serologic status of horses can affect their import status. Therefore, the serologic status of breeding horses should be determined before vaccination, and all subsequent vaccinations should be recorded. (See also Equine Viral Arteritis.)
Potomac horse fever (see Potomac Horse Fever) caused by Ehrlichia risticii may be followed by abortion in mid- to late gestation. There is placentitis and the placenta is often retained. The organism has been isolated from fetal lymphoid tissues after abortion. Histologically, there is fetal colitis. Identification of this colitis provides a presumptive diagnosis. There is a vaccine for Potomac horse fever, but its efficacy in preventing abortion is not known.
Leptospirosis has recently been recognized as an important cause of sporadic equine abortion in Kentucky, Northern Ireland, and England. Most fetuses are aborted after 6 mo of gestation and the mares are usually healthy. Infection does not appear to spread horse-to-horse, and often only a single mare on a farm aborts. There are no gross lesions in the fetus or placenta, but microscopically there is suppurative placentitis. Diagnosis is by fluorescent antibody staining of placenta or fetal kidney, liver, or lung and by fetal serology. A large majority of the cases in Kentucky are caused by Leptospira interrogans serovar pomona type kennewicki, although other serovars have also been identified.
Abortion due to Streptococcus zooepidemicus, other Streptococcus spp, Salmonella, Escherichia coli, Pseudomonas, Klebsiella, or other bacteria usually is caused by an ascending infection through the cervix that results in placentitis. The placenta is edematous with brown fibrinonecrotic exudate near the cervical star. Chronic placentitis results in retardation of fetal growth. The fetus may be severely autolyzed when expelled. Organisms can be recovered from aseptically obtained stomach contents.
Equine Mycotic Placentitis
Mycotic placentitis in horses is also due to an ascending infection that causes a thickened chorioallantois with variable exudate. Causative agents include Aspergillus, Mucor, and Candida. Fetuses aborted in late gestation may be fresh, with evidence of growth retardation. A pale, enlarged liver or dermatitis may be found. Hyphae are found in the placenta, liver, lungs, or stomach contents.
Last full review/revision July 2011 by Jerome C. Nietfield, DVM, PhD, DACVP