Clinical Theriogenology 2022; 14: 50 Introduction Equine theriogenology is focused on the production of a live foal. Infertility in horses is common and only ~ 67% of mares produce a live foal.1 Number of mares becoming pregnant and producing a live foal is increasing;2,3 however, failure of preg- nancy (FOP) has been an important impediment to produce a live foal. In camelids, estimates are not readily available. Investigations of FOP in horses is a most rewarding diagnos- tic experience because success rate is very high (83 - 93%),4- 7 higher than other species. Camelids, in contrast, like other species, have a success rate of up to 50%.8 Major difference between horses and other species is the commonality of non- infectious causes in horses that can be identified by lesions visible at gross/macroscopic evaluation. This will be the focus in this review. Failure of pregnancy in horses and camelids is described in detail in review articles, textbook chapters, symposium pro- ceedings, and diagnostic laboratory pamphlets. Most diag- nostic laboratories have a procedure, protocol, and/or list of diagnostic samples to aid in identifying infectious FOP in horses and to a lesser extent, in camelids. Most reviews and descriptions follow a familiar theme; separation of causes of FOP into infectious causes and everything else is based on the ease with which diagnostic laboratories can process samples to identify microbial agents. In camelids, most FOP cases are considered idiopathic; they have no infectious causes and have no lesions. Many reports Failure of pregnancy in horses and camelids Robert Foster Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, Ontario, Canada Abstract Determining pregnancy failures in horses and camelids is approached as a diagnostic investigation of an individual animal. It begins with the preliminary discussion around expectations of the investigation and apparently, diagnostic success rate is high in horses. However, diagnostic success in camelids is low. General approach from a pathology point of view is to identify several of noninfectious fetal and fetal membranes’ lesions and then determine the potential infectious causes; agents include viruses, eubacteria, protozoa, and fungi. Bacterial and fungal infections are mostly ascending infections whereas viral and protozoal are systemic infections. When an infectious cause is excluded, the focus is directed on potential noninfectious causes and particularly those with detectible lesions. Maternal evaluation, specifically, via endometrial biopsy and examination of fetus and fetal mem- branes (including umbilical cord) in horses, normally provide an explanation for noninfectious failure of pregnancy in several circumstances. Special attention should be given to fetal thyroid gland, tracheal contents, and musculoskeletal system, particularly, the medulla of long bones. In horses, noninfectious failure of pregnancy with no lesions (idiopathic abortion) is observed in a small percentage of cases. In camelids, it is a common ‘diagnosis.’ Keywords: Horses, camelids, pregnancy, abortion, stillbirth, embryonic mortality on causes of FOP are based on sample submissions to diag- nostic laboratories.4,5,6,9 This approach is logical and practical. Overlying this is the division of causes into those with identi- fiable lesions or those with no lesions. Fortunately, the num- ber of cases in horses where there are neither infectious agents nor lesions identified (idiopathic FOP) is very low. Further- more, causes are classified (based on origin) into maternal, fetal, or placental. Paternal causes possibility is also included in this review. The intention is not to replicate work already presented, but rather to highlight some important aspects and lesions that are easy to miss at macroscopic and microscopic evaluation. Additionally, ‘idiopathic’ failure of pregnancies is considered. General approach to failure of pregnancy There are 2 parts to the general approach to FOP. Preliminary discussions with owners to ensure safety, reasonable expecta- tions, and thorough evaluation. Second, the diagnostic pro- cess. Preliminary discussions begin before the diagnostic process and normally, includes discussing public health and safety issues, identifying the problem, performing a cost-benefit analysis of investigation and diagnosis, and discussing quar- antine efforts of affected dams. In horses and camelids in North America, public health issues are minimal and in gen- eral, equine fetal membranes are not regarded as biohazard- ous above Level 2. Because horses and camelids are treated as Clinical Theriogenology 2022; 14: 51 individuals, attempts for them to become pregnant and give birth are costly, there is usually a benefit for evaluation par- ticularly, in horses where the diagnosis rate is so high. High- ly infectious nature of equid alphaherpesvirus 1 (commonly known as equine herpesvirus 1; EHV-1) in horses means that every case should be evaluated for viral presence. This alone is a major focus in FOP investigation in horses even though the prevalence of EHV-1 in diagnostic material is relatively low and is ~ 3 or 4% in several large studies.4-7,10,11 Diagnostic process is like any other disease investigation and involves determining signalment, history, macroscopic eval- uation, and collection of samples from the mare, fetus and fetal membranes, ancillary testing, and arriving at a diagno- sis. Careful evaluation of fetus and fetal membranes and the collection of appropriate samples as outlined by a particular diagnostic laboratory must be carried out for complete eval- uation. During this process of sample collection, it is very important to have complete evaluation of all parts of fetal membranes and umbilical cord. When performing a postmortem exam- ination on an equine fetus, evaluate thyroid gland, examine tracheal and bronchial contents, include skeletal muscle and sectioning of long bones. Reporting findings is now greatly enhanced by taking photographs with a mobile phone; this is sufficiently helpful when seeking opinions from diagnostic and or reproductive pathologists or equine theriogenologists. Careful macroscopical evaluation is very useful in identifying several noninfectious causes of FOP that in the horse repre- sent 30 – 40% of overall causes.4-7,10,11 Infectious causes of failure of pregnancy Infectious causes in horses account ~ 40% of the causes of FOP.4-7,10,11Stud owners give greater importance to equid al- phaherpesvirus 1 because it is believed to have high infective- ness and has a propensity to move rapidly through a group of horses. However, it has not been a major infectious cause of FOP.4-7,10,11 Placentitis, either in the region of the ‘cervical star’ or in the body portion of fetal membranes (in nocardioform placenti- tis12), is a common lesion that when present is highly likely the cause of FOP; amnionitis is also a distinct lesion. Approximately 70% of cases of placentitis have a microbe identified as the potential cause.12,13 Majority of infectious causes of FOP are bacteria, and most common bacterial spe- cies are Streptococcus equi zooepidemicus or gram-negative or- ganisms. These usually infect fetal membranes by ascending through the cervix. There are several potential bacteria that can cause FOP by the transcervical route. Other bacteria (e.g. nocardioform actinomycetes) are usually sporadic.14 Bacteria that infect fetus and fetal membranes include Lepto- spira interrogans, Neorickettsia risticii, Borrelia burgdorferi, Chla- mydia psittaci, mycobacteria, and less commonly mycoplasma and Coxiella burnetii. Horses and camelids can be infected with these bacteria. Fungal, protozoal, and viruses (other than equid alphaherpes- virus 1) are sporadic causes that can be recovered from diag- nostic specimens with modern techniques particularly, molec- ular types (e.g. polymerase chain reaction-based assays). Endometritis, including infectious endometritis, postbreed- ing endometritis, and postpartum endometritis all potentially contribute to FOP and infertility in mares. It results in em- bryonic mortality, particularly, early embryonic mortality.15,16 Important components in the development of endometritis include variations in physical clearance and uterine tone, non- adaptive molecular immune response, and nonadaptive cellu- lar immune response; these are areas of active research. Uterine clearance and tone are especially important and sys- tems to measure clearance and tone are being developed. Active inflammation of the endometrium is best detected by cytology and the effects of inflammation of the endometrium via endometrial biopsy. Endometrial biopsy continues to be an important method of prognosis for fertility in mares.17-20 Evaluation of the mare is an important component of evaluat- ing FOP; however, in middle or last third of pregnancy losses, the mare is often overlooked as a source of information about the fetomaternal interface and potential infectious agents. As with mares, camelids can be sampled for endometrial biopsy and this is a valuable adjunct to evaluation of infertility and FOP. Amnionitis and funisitis is a unique presentation of infection in horses. Whereas a variety of bacteria can be recovered, the underlying process in the cause of disease, variously known as ‘mare reproductive loss syndrome’ or equine amnionitis, and fetal loss, was determined to be from the transmigration of setae of processionary caterpillars.21-27 Noninfectious causes of failure of pregnancy Noninfectious causes of FOP represent a substantial compo- nent of the overall causes, ~ 50%. These causes can be classified into fetal, placental, maternal, fetomaternal incompatibility, and paternal components. Several of these have identifiable lesions whereas some lack. Noninfectious causes are classified into those with identifiable lesions and those without lesions. This aids in the investigation of the problem at the herd level. Noninfectious causes with lesions Noninfectious lesions of the mare, fetus, and fetal membranes are often identifiable at gross or macroscopic evaluation; how- ever, some require careful evaluation of fetus and fetal mem- branes. Noninfectious fetal lesions Some lesions are highly visible congenital defects, and include hydrocephalus, craniofacial anomalies, schistosomus reflexus, and various musculoskeletal defects including arthrogryposis and angular limb deformities. Fetal neoplasia such as hepa- toblastoma,28,29 although extremely rare, is often very remark- able and do not present a challenge. Clinical Theriogenology 2022; 14: 52 Dystocia or birth trauma have fetal abnormalities without routine histological changes and can only be determined at postmortem. Twinning once was a major cause of FOP in mares10 but is now uncommon. It was diagnosed as a cause of FOP based on gross examination of the fetuses and fetal membranes. Causes with a histologic lesion but no gross lesion requires collection of the appropriate sample. Approximately 3% of foals with glycogen branching enzyme deficiency are aborted and histological evaluation of muscle is required.30 Thyroid hy- perplasia observed with and without musculoskeletal disease, and thyroid hyperplasia/congenital hypothyroidism-dysma- turity syndrome requires microscopic evaluation of the thy- roid gland for diagnosis. Thyroid histology must be combined with evaluation of long bones to detect osteopetrosis in those cases that do not have skeletal abnormalities such as man- dibular prognathia, inappropriately ossified carpal and tar- sal bones, flexural deformities of the forelimbs and ruptured tendons of the common digital extensor muscles.31-34 Giant cell hepatopathy35 is a lesion of unknown cause identified in aborted fetuses that have no other identifiable causes of FOP. In camelids, anomalies of the head are the most common, especially choanal stenosis. Cardiac anomalies are also report- ed. Noninfectious umbilical and fetal membranes’ lesions Examination of fetal membranes and umbilicus in equine FOP is a rewarding and reassuring experience once the investi- gator is familiar with normal fetal membranes and umbilical cord.36, 37 Macroscopic evaluation of fetal membranes and umbilical cord in horses should always begin with measurement of the cord for length, as excessively long or excessively short cords cause FOP. The length of cord varies among ponies, Thoroughbreds and Standardbreds, and draft breeds. For Thoroughbreds and Standardbreds there is some variation in what is considered the normal reference range and the gener- al figures38 of 36 - 83 cm is a good guide. Cords that are too short can potentially rupture or pull fetal membranes from the endometrium at the insertion of the cord.39 Cords that are too long may have greater resistance to blood flow, become strangulated and wrap around a limb, the neck or the body, develop excessive torsion or develop an infarct of the placen- ta.6,39,40 Excessive twists that are substantial may have evidence of torsion, particularly edema of the umbilical cord and di- lation of the urachus. Other abnormalities of the umbilical cord include a single umbilical artery9,41 strangulation(s) by the yolk sac remnant, a knot in the umbilical cord, umbilical hernia into the umbilical cord or the lesions of amnionitis and funisitis as occurs in mare reproductive loss syndrome/ equine amnionitis and fetal loss. Camelids normally have a relatively long cord, and torsion and strangulation(s) occur sporadically.42 Ingestion by mares of processionary caterpillars begins as a noninfectious process however the setae of the caterpillars move through the intestines into the uterus and placenta car- rying with them various types of microbes.26,27 Limited infor- mation is available regarding pathogenesis of hydrallantois and hydramnios in mares for clinically obvious reasons.43 An abnormal site of attachment of the embryo to the uterus resulting in an umbilical cord attached to the body of the uter- us results in body pregnancy and fetal loss. Formation of body pregnancy is an anomaly (limited information is known) and research in equine embryo attachment to the endometrium may provide insights in this area.44 Currently, placental edema and prolonged pregnancy follow- ing ingestion of mycotoxins as part of fescue endophyte toxi- coses,45,46 occurs sporadically. Nutrition of the fetus and fetal membranes via endometrium occurs through a combination of histotrophic and hemo- trophic means.47 Secretions of endometrial glands are re- quired for the uterine ‘milk’ that is taken up by trophoblasts at the base of the microcotyledons. Adequate microcotyledonary surface area is required for hemotrophic transfer. Endometri- al disease, particularly, fibrosis and alteration of endometrial glands, is likely to alter placental development and the result- ing reduced gland secretion, transfer of nutrients and surface area. Endometrial biopsy is the only effective way to measure alteration to endometrial structure that could influence pla- cental surface area. Quantitative means to measure surface area in a diagnostic setting is not established. Endometrial biopsy therefore remains an important component of investi- gation of FOP and infertility in horses and camelids. Twinning reduces the surface area of each placenta and is re- sponsible for FOP. Twinning is now an unusual finding be- cause of early detection and clinical intervention. It is more common in those animals that were not subjected to preg- nancy testing. The prevalence of twinning is ~ 0.1% of preg- nancies.48 Noninfectious causes without lesions The most difficult group to identify as the cause of FOP are those that are noninfectious, and which do not have lesions identifiable either macroscopically or microscopically. This is the group that includes maternal causes, fetomaternal in- compatibilities and those causes that have toxic, nutritional, genetic or molecular anomalies. Maternal causes may be readily identifiable and as such, fetal and placental examination may be done on farm but not sent to diagnostic laboratories. Thus, maternal illness seldom is included in laboratory statistics. Colic is a recognized predis- posing factor for FOP.49-51 Age of mare,10,52 failure of a previous pregnancy,10 endometritis,53 endometrial fibrosis,18,54 uterine neoplasia,55 and hormonal failure 2,56 are all reported. It is generally considered that the majority of genetic or mo- lecular causes of FOP are responsible for embryonic mortali- ty and return to estrus. It is variously called repeat early em- bryonic loss, equine early embryonic loss or early pregnancy loss.57,58 Cases lacking macroscopic or microscopic abnormali- ties have no known cause, partially because routine evaluation of chromosomal or molecular abnormalities is not available. Clinical Theriogenology 2022; 14: 53 There are some reports of chromosomal abnormalities in the fetus including mosaicism 51 or chromosomal or molecular abnormalities in mares, including single nucleotide polymor- phism60 or chromosomal translocations.61 This is a field where ongoing research is necessary. Paternal causes of FOP have received limited attention. It has long been recognized that some stallions have an abortion rate that is higher than others10 but there is limited research in this area. Conclusion Diagnosis of FOP, especially in the mare, is a rewarding pro- cess with a very high rate of diagnostic success. A search for noninfectious causes including placental and umbilical cord lesions, and evaluation for unique diseases in mares and fe- tuses, particularly, bone, muscle, and thyroid tissues, increases the diagnostic success rate even further. Conflict of interest Author has no conflict of interest and no funding was received for this publication. References 1. Lane EA, Bijnen M, Osborne M, et al: Key Factors Affecting Reproductive Success of Thoroughbred Mares and Stallions on  a Commercial Stud Farm. Reprod Domest Anim 2016;51:181-187. 2. Allen WR, Wilsher S: Half a century of equine reproduction research and application: A veterinary tour de force. Equine Vet J. 2018;50:10- 21. 3. Rose BV, Firth M, Morris B, et al: Descriptive study of current therapeutic practices, clinical reproductive findings and incidence of pregnancy loss in intensively managed thoroughbred mares. Anim Reprod Sci 2018;188:74-84. 4. Giles RC, Donahue JM, Hong CB, et al: Causes of abortion, stillbirth, and perinatal death in horses: 3,527 cases (1986-1991). J Am Vet Med Assoc 1993;203:1170-1175. 5. Hong CB, Donahue JM, Giles RC Jr, et al: Equine abortion and stillbirth in central Kentucky during 1988 and 1989 foaling seasons. J Vet Diagn Invest 1993;5:560-566. 6. Smith KC, Blunden AS, Whitwell KE, et al: A survey of equine abortion, stillbirth and neonatal death in the UK from 1988 to 1997. Equine Vet J 2003;35:496-501. 7. Roach JM, Foote AK, Smith KC, et al: Incidence and causes of pregnancy loss after day 70 of gestation in Thoroughbreds. Equine Vet J 2021;53:996-1003. 8. Schaefer DL, Bildfell RJ, Long P, et al: Characterization of the microanatomy and histopathology of placentas from aborted, stillborn, and normally delivered alpacas (Vicugna pacos) and llamas (Lama glama). Vet Pathol 2012;49:313-321. 9. Marenzoni ML, Lepri E, Casagrande Proietti P, et al: Causes of equine abortion, stillbirth and neonatal death in central Italy. Vet Rec 2012;170:262. 10. Platt H: Aetiological aspects of abortion in the thoroughbred mare. J Comp Pathol 1973;83:99-205. 11. Tengelsen LA, Yamini B, Mullaney TP, et al: A 12-year retrospective study of equine abortion in Michigan. J Vet Diagn Invest 1997;9:303- 306. 12. Hong CB, Donahue JM, Giles RC Jr, et al: Etiology and pathology of equine placentitis. J Vet Diagn Invest 1993;5:56-63. 13. Canisso I, Ball BA, Squires EL, et al: Comprehensive review on equine placentitis. Proc Am Assoc Equine Pract 2015; p. 490-509. 14. Tibary A, Fite C, Anouassi A, et al: Infectious causes of reproductive loss in camelids. Theriogenology 2006;66:633-647. 15. Woodward EM, Troedsson MH: Inflammatory mechanisms of endometritis. Equine Vet J 2015;47:384-389. 16. Morris LHA, McCue PM, Aurich C: Equine endometritis: a review of challenges and new approaches. Reproduction 2020;160:R95-R110. 17. Gordon LR, Sartin EM: Endometrial biopsy as an aid to diagnosis and prognosis in equine infertility. J Equine Med Surg 1978;2:328- 336. 18. Kenney RM, Doig PA: Equine endometrial biopsy, In: Current Therapy in Theriogenology 2. Philadelphia; WB Saunders: 1986. p.723-729. 19. Schlafer DH: Equine endometrial biopsy: enhancement of clinical value by more extensive histopathology and application of new diagnostic techniques? Theriogenology 2007;68:413-422. 20.Snider TA, Sepoy C, Holyoak GR: Equine endometrial biopsy reviewed: observation, interpretation, and application of histopathologic data. Theriogenology 2011;75:1567-1581. 21. Sebastian MM, Bernard WV, Riddle TW, et al: Review paper: mare reproductive loss syndrome. Vet Pathol 2008;45:710-722. 22. Todhunter KH, Perkins NR, Wylie RM, et al: Equine amnionitis and fetal loss: the case definition for an unrecognised cause of abortion in mares. Aust Vet J 2009;87:35-38. 23. McDowell KJ, Webb BA, Williams NM, et al: Invited review: the role of caterpillars in mare reproductive loss syndrome: a model for environmental causes of abortion. J Anim Sci 2010;88: 1379-1387. 24. Cawdell-Smith AJ, Todhunter KH, Anderson ST, et al: Equine amnionitis and fetal loss: mare abortion following experimental exposure to Processionary caterpillars (Ochrogaster lunifer). Equine Vet J 2012;44:282-288. 25. Cawdell-Smith AJ, Todhunter KH, Perkins NR, et al: Exposure of mares to processionary caterpillars (Ochrogaster lunifer) in early pregnancy: An additional dimension to equine amnionitis and fetal loss. Equine Vet J 2013;45:755-760. 26. Todhunter KH, Cawdell-Smith AJ, et al: Processionary caterpillar setae and equine fetal loss: Histopathology of the fetal-placental unit from experimentally exposed mares. Vet Pathol 2014;51:1131-1142. 27. de Vries C, Vanhaesebrouck E, Govaere J, et al: Congenital ascites due to hepatoblastoma with extensive peritoneal implantation metastases in a premature equine fetus. J Comp Pathol 2013;148:214- 219. 28. Neu SM: Hepatoblastoma in an equine fetus. J Vet Diagn Invest. 1993; 5: 634-637. 29. Render JA, Common RS, Kennedy FA, et al: Amylopectinosis in fetal and neonatal Quarter Horses. Vet Pathol 1999;36:157-160. 30. Allen A: Hyperplasia of the thyroid gland and musculoskeletal deformities in two equine abortuses. Can Vet J 1995;36:234-236. Clinical Theriogenology 2022; 14: 54 31. Allen AL, Doige CE, Fretz PB, et al: Hyperplasia of the thyroid gland and concurrent musculoskeletal deformities in western Canadian foals: reexamination of a previously described syndrome. Can Vet J 1994;35:31-38. 32. Allen AL, Townsend HG, Doige CE, et al: A case-control study of the congenital hypothyroidism and dysmaturity syndrome of foals. Can Vet J 1996;37:349-351;354-358. 33. Koikkalainen K, Knuuttila A, Karikoski N, et al: Congenital hypothyroidism and dysmaturity syndrome in foals: First reported cases in Europe. Equine Vet Educ 2014;26:181-189. 34. Car BD, Anderson WI. Giant cell hepatopathy in three aborted midterm equine fetuses. Vet Pathol 1988;25:389-391. 35. Pozor M: Equine placenta – A clinician’s perspective. Part 2: Abnormalities. Equine vet Educ 2016;28:394-404. 36. Prickett ME: Abortion and placental lesions in the mare. J Am Vet Med Assoc 1970;157:1465-1470. 37. Whitwell KE, Jeffcott LB: Morphological studies on the fetal membranes of the normal singleton foal at term. Res Vet Sci 1975;19:44-55. 38. Whitwell KE: Morphology and pathology of the equine umbilical cord. J Reprod Fertil 1975;23(Suppl):599-603. 39. Foote AK, Ricketts SW, Whitwell KE: A racing start in life? The hurdles of equine feto-placental pathology. Equine Vet J 2012;41(Suppl):120-129. 40. Girodroux M, Lores M, Vilaregut L, et al: A single umbilical artery and omphalophlebitis in an Arabian foal. Equine Vet Educ 2019;31:6- 12. 41. Johnson LW: Llama reproduction. Vet Clin North Am Food Anim Pract 1989;5:159-182. 42. Mitchell ARM, Delvescovo B, Tse M, et al: Successful management of hydrallantois in a Standardbred mare at term resulting in the birth of a live foal. Can Vet J 2019;60:495-501. 43. Quinn BA, Hayes MA, Waelchli RO, et al: Changes in major proteins in the embryonic capsule during immobilization (fixation) of the conceptus in the third week of pregnancy in the mare. Reproduction 2007;134:161-170. 44. Putnam MR, Bransby DI, Schumacher J, et al: Effects of the fungal endophyte Acremonium coenophialum in fescue on pregnant mares and foal viability. Am J Vet Res 1991;52:2071-2074. 45. Riet-Correa F, Rivero R, Odriozola E, et al: Mycotoxicoses of ruminants and horses. J Vet Diagn Invest 2013;25:692-708. 46. Bastos HBA, Martinez MN, Camozzato GC, et al: Proteomic profile of histotroph during early embryo development in mares. Theriogenology 2019;125: 224-235. 47. Anaya G, Fernández ME, Valera M, et al: Prevalence of twin foaling and blood chimaerism in purebred Spanish horses. Vet J 2018;234:142-144. 48. Santschi EM, Slone DE, Gronwall R, et al: Types of colic and frequency of postcolic abortion in pregnant mares: 105 cases (1984- 1988). J Am Vet Med Assoc 1991;199:374-377. 49. Boening KJ, Leendertse IP: Review of 115 cases of colic in the pregnant mares. Equine Vet J 1993;25:518-521. 50. Chenier TS, Whitehead AE: Foaling rates and risk factors for abortion in pregnant mares presented for medical or surgical treatment of colic: 153 cases (1993-2005). Can Vet J 2009;50:481-485. 51. Bain AM: Foetal losses during pregnancy in the thoroughbred mare: a record of 2,562 pregnancies. N Z Vet J 1969;17:155-158. 52. Darenius K: Early foetal death in the mare. Histological, bacteriological and cytological findings in the endometrium. Acta Vet Scand 1992;33:147-160. 53. Waelchli RO: Endometrial biopsy in mares under nonuniform breeding management conditions: Prognostic value and relationship with age. Can Vet J 1990;31:379-384. 54. Canisso IF1, Pinn TL, Gerdin JA, et al: B-cell multicentric lymphoma as a probable cause of abortion in a Quarter horse broodmare. Can Vet J 2013;54:288-291. 55. Allen WR, S. Wilsher S: Persistent endometrial cups in the same mare in two successive pregnancies. Equine Vet Educ 2012;24:247- 250. 56. Wilsher S: The uterus and early pregnancy failure in the mare. Equine Vet Educ 2019;31:214-224. 57. Kahler A, McGonnell IM, Smart H, et al: Fetal morphological features and abnormalities associated with equine early pregnancy loss. Equine Vet J 2020;53:530-541. 58. Whitwell KE: Investigations into fetal and neonatal losses in the horse. Vet Clin North Am Large Anim Pract 1980;2:313-331. 59. Leon PM, Campos VF, Thurow HS, et al: Association between single nucleotide polymorphisms in p53 and abortion in Thoroughbred mares. Vet J 2012;193:573-575. 60. Ghosh S, Das PJ, Avila F, et al: A non-reciprocal autosomal translocation 64,XX, t(4;10)(q21;p15) in an Arabian mare with repeated early embryonic loss. Reprod Domest Anim 2016;51:171- 174.