Equine placenta – A clinician's perspective. Part 1: Normal placenta – Physiology and evaluation

A complex organ, the equine placenta is responsible for fetal nourishment, protection from external and internal insults, and the production and/or metabolisation of various hormones. The endometrial cups are unique structures of the equine placenta that are responsible for producing an essential hormone for equine pregnancy, equine chorionic gonadotropin. Since mares have epitheliochorial placentae, with 6 layers of tissue separating maternal from fetal circulation, almost the entire surface of the chorioallantois must be attached to the maternal endometrium in order to support a developing fetus adequately. The only avillous areas of the normal chorioallantois are: the cervical star, sites of the endometrial cups, areas facing oviductal papillae, folds overlying major allantoic vessels, and fetal foot PADs (placental areas of degeneration). There are characteristic differences between the gravid and the nongravid horn of the chorioallantois. Allantoic vesicles, allantoic pouches, hippomanes, amniotic plaques and yolk sac remnants are normal features of the equine placenta. The clinician should thoroughly examine the entire placenta immediately after its expulsion. The most important aspect of this evaluation is to check for completeness of the chorioallantois, along with identifying any pathological lesions on the fetal membranes or the umbilical cord.     

Equine amnionitis and fetal loss: mare abortion following experimental exposure to Processionary caterpillars (Ochrogaster lunifer)

Reasons for performing study: In Australia, there have been recent reports of unusual abortions in mid‐ to late‐gestation mares. These were clinically distinct from other recognised causes of pregnancy loss and the term ‘equine amnionitis and fetal loss’ (EAFL) was adopted to describe this syndrome. Initial investigations concluded that possible causal factors included the presence on affected stud farms of Processionary caterpillars (Ochrogaster lunifer). Objectives: To determine if exposure of pregnant mares to Processionary caterpillars or their shed exoskeletons can induce EAFL. Methods: Processionary caterpillars and their shed exoskeletons were collected and stored frozen. Mid‐gestation mares were dosed with a slurry of caterpillars or shed exoskeleton by nasogastric intubation. Their clinical responses and times to abortion were recorded. All aborted fetuses were autopsied and samples taken for bacteriological and virological culture and histopathology. Results: Intubating mares in mid‐pregnancy with preparations of either whole Processionary caterpillars or shed caterpillar exoskeletons induced abortion with few impending clinical signs. The gross pathological and bacteriological findings of the aborted fetuses were similar to those observed in field cases of EAFL. Potential relevance: Possible exposure to Processionary caterpillars should be considered when examining cases of fetal loss in the mare. The present results provide a starting point to further explore the aetiology and pathogenesis of EAFL.     

Equine clinical genomics: A clinician's primer

The objective of this review is to introduce equine clinicians to the rapidly evolving field of clinical genomics with a vision of improving the health and welfare of the domestic horse. For 15 years a consortium of veterinary geneticists and clinicians has worked together under the umbrella of The Horse Genome Project. This group, encompassing 22 laboratories in 12 countries, has made rapid progress, developing several iterations of linkage, physical and comparative gene maps of the horse with increasing levels of detail. In early 2006, the research was greatly facilitated when the US National Human Genome Research Institute of the National Institutes of Health added the horse to the list of mammalian species scheduled for whole genome sequencing. The genome of the domestic horse has now been sequenced and is available to researchers worldwide in publicly accessible databases. This achievement creates the potential for transformative change within the horse industry, particularly in the fields of internal medicine, sports medicine and reproduction. The genome sequence has enabled the development of new genome‐wide tools and resources for studying inherited diseases of the horse. To date, researchers have identified 11 mutations causing 10 clinical syndromes in the horse. Testing is commercially available for all but one of these diseases. Future research will probably identify the genetic bases for other equine diseases, produce new diagnostic tests and generate novel therapeutics for some of these conditions. This will enable equine clinicians to play a critical role in ensuring the thoughtful and appropriate application of this knowledge as they assist clients with breeding and clinical decision‐making.     

Retained Fetal Membranes in Heavy Draft Mares Associated with Histological Abnormalities

Retention of fetal membranes is one of the most common life-threatening peripartum problems; however, its etiology is still unknown. Draft mares are more likely to retain fetal membranes than other breeds of mares. Because a strong connection between the fetal membranes and the endometrium has been observed in cases of retention, we studied the changes in the endometrium and the allantochorion of heavy draft mares with this condition. Tissue samples were taken from 90 mares that retained the fetal membranes and from 21 that did not. Retained fetal membranes were associated with adhesion of the allantochorion to the endometrium in 88% of the mares; this adhesion depended on the following factors: occurrence of fibrosis both in the lamina propria of the allantochorial villi and in the allantochorial stromal connective tissue, overdevelopment of the allantochorial stromal connective tissue, oversized allantochorial epithelial cells, and sparser and less-branched allantochorial villi.     

Rethinking equine gastric ulcer syndrome: Part 2 – Equine squamous gastric ulcer syndrome (ESGUS)

It has recently been highlighted that significant differences in prevalence, risk factors and the response to treatment exist between ulceration of the squamous gastric mucosa and ulceration of the glandular gastric mucosa in the horse. In the first article in the series, the term equine squamous gastric ulcer syndrome (ESGUS) was used to describe disease of the squamous gastric mucosa with clinical signs and diagnosis discussed. The purpose of this article is to review the pathophysiology, risk factors, prevalence, treatment and prevention of ESGUS.     

Rethinking equine gastric ulcer syndrome: Part 3 – Equine glandular gastric ulcer syndrome (EGGUS)

It has recently been highlighted that significant differences exist between ulceration of the squamous gastric mucosa and ulceration of the glandular gastric mucosa in the horse. The first article in this series discussed terminology, clinical signs and diagnosis and the second reviewed ulceration of the squamous gastric mucosa in detail. The purpose of this article, the third and last in the series, is to review the pathophysiology, risk factors, prevalence, treatment and prevention of ulceration of the glandular gastric mucosa.     

Prostaglandins F2α and E2 in rat placenta and fetal membrane: a comprehensive immunohistochemistry of their synthetic enzymes and in vivo tissue levels during normal pregnancy

We determined a comprehensive immunohistochemistry of putative isoforms of enzymes for prostaglandin (PG) F₂α and PGE₂ biosynthesis and these PGs levels in placenta and fetal membrane of normal pregnant rats in vivo. Placenta and fetal membrane showed positive immunoreactions for phospholipase A₂ group 4A, but not group 2A, and cyclooxygenase (COX)-1 rather than COX-2. They showed positive immunoreactions for at least one isoform of each of PGF synthase and PGE synthase with tissue-dependent variations. PGF₂α and PGE₂ levels in both tissues were highest on day 12 and declined and remained low thereafter. Obtained data would be the basic information on the primary PGs synthesis in rat placenta and fetal membrane in normal pregnancy.     

Spurious hypercreatininemia: 28 neonatal foals (2000–2008)

Objectives – To (1) determine the occurrence of spurious hypercreatininemia in a population of hospitalized foals <2 days old, (2) assess the resolution of the hypercreatininemia, and (3) determine its association with survival in these foals. Design – Retrospective case series. Setting – 2 Referral hospitals. Animals – Foals <2 days old with an admission creatinine >442 μmol/L (>5.0 mg/dL) from 2 referral hospitals. Interventions – None. Measurements and Main Results – The medical records of 33 foals were reviewed. Twenty‐eight had spurious hypercreatininemia and 5 had acute renal failure. Admission creatinine was not significantly different between the 2 groups (mean [standard deviation]). The creatinine was 1,202 μmol/L (663 μmol/L) (13.6 mg/dL [7.5 mg/dL]) versus 1,185 μmol/L (787 μmol/L) (13.4 mg/dL [8.9 mg/d]) (P=0.96) in each group, respectively, though BUN at the time of hospital admission was significantly higher for acute renal failure foals (P=0.009). In the spurious group, serum creatinine at admission decreased to 504 μmol/L (380 μmol/L) (5.7 mg/dL [4.3 mg/dL]) by 24 hours, and to 159 μmol/L (80 μmol/L) (1.8 mg/dL [0.9 mg/dL]) at 48 hours, and to 115 μmol/L (44 μmol/L) (1.3 mg/dL [0.5 mg/dL]) at 72 hours. Twenty‐three of 28 foals with spurious hypercreatininemia survived to hospital discharge and there was no difference in mean admission creatinine between survivors (1176 μmol/L [628 μmol/L]) (13.3 mg/dL [7.1 mg/dL]) and nonsurvivors (1308 μmol/L [857 μmol/L]) (14.8 mg/dL [9.7 mg/dL]) (P=0.67). Twenty of 28 foals had clinical signs suggestive of neonatal encephalopathy. Conclusion – Creatinine decreased by >50% within the initial 24 hours of standard neonatal therapy and was within the reference interval in all but 1 foal within 72 hours of hospitalization. The diagnosis of neonatal encephalopathy was common in these foals.     

Equine proliferative enteropathy – a review of recent developments

Equine proliferative enteropathy (EPE) is a disease of foals caused by the obligate intracellular organism Lawsonia intracellularis. This emerging disease affects mainly weanling foals and causes fever, lethargy, peripheral oedema, diarrhoea, colic and weight loss. The diagnosis of EPE may be challenging and relies on the presence of hypoproteinaemia, thickening of segments of the small intestinal wall observed upon abdominal ultrasonography, positive serology and molecular detection of L. intracellularis in faeces. Although the clinical entity, diagnostic approach and treatment of EPE are well established and described, the epidemiology for this disease has remained largely unaddressed. This article focuses on new developments in the field of EPE, including epidemiology, pathophysiology, clinical signs, diagnosis, treatment and prevention. The Summary is available in Chinese – see Supporting information.     

Evaluation of poor performance in competition horses: A musculoskeletal perspective. Part 2: Further investigation

There is not a right and a wrong way of investigating musculoskeletal causes of poor performance in sports horses and the methods of investigation are, in part, determined by the clinical signs. Measurement of serum muscle enzyme concentrations before and after exercise is essential for recognition of primary muscle pathology. Many horses with multilimb lameness have a secondary reduced range of motion of the thoracolumbosacral region mimicking primary thoracolumbar pain. Radiographic examination of the thoracolumbar vertebrae may be confusing unless combined with diagnostic analgesia because many clinically normal horses have radiological abnormalities. Nuclear scintigraphy offers a method of evaluating a large proportion of the horse, but there are many false positive and false negative results. Diagnostic analgesia is the most reliable method of investigation but requires experience and skill in interpretation and is time consuming in a horse with multilimb lameness.     

Rethinking equine gastric ulcer syndrome: Part 1 – Terminology,clinical signs and diagnosis

Equine gastric ulcer syndrome (EGUS) is a common condition in the horse. A series of recent articles highlighting differences in healing of squamous and glandular ulceration have reinvigorated interest in the condition. The purpose of this series of articles is to review the current thinking on EGUS with particular emphasis on the differences between diseases of the squamous and glandular mucosae. This article, the first will review the terminology, clinical signs and diagnosis of EGUS in the horse.     

The aetiopathogenesis of equine periodontal disease – a fresh perspective

Periodontal disease is a painful and highly prevalent disorder of horses that causes a significant welfare problem. Despite its importance, few scientific studies on its aetiopathogenesis have been performed. Equine periodontitis differs from the plaque‐induced periodontitis found in brachydont species where bacteria accumulating in dental plaque induce a destructive inflammatory response in the periodontium. In contrast, equine periodontitis is usually initiated by entrapment of feed between cheek teeth, which causes inflammation of periodontal tissue that likely allows bacterial infection of the periodontal tissues that is later exacerbated by the host's response. Equine oral microbiology is a neglected field of research and identification of the bacteria involved in this disorder by use of molecular bacteriology and examination of the interaction between these bacteria and the equine oral immune response should reveal important information about the pathogenesis of this disease.     

Management of equine ataxia caused by cervical vertebral stenotic myelopathy: A European perspective 2010–2015

The diagnosis and therapy of cervical vertebral stenotic myelopathy (CVSM) are challenging and have been most frequently described in racehorses. We aimed to analyse CVSM cases presented for diagnostic work‐up and treatment in a nonracing horse population. We hypothesised that our diagnostic work‐up protocol including clinical/orthopaedic/neurological/radiographic and myelographic examinations may provide practical reference points for in vivo diagnosis/prognosis and adequate CVSM management. Medical records from 2010 to 2015 were reviewed retrospectively. Cases were included if our standardised work‐up protocol was followed, there was no evidence of any infectious diseases causing the neurological signs, and native cervical radiographs and myelograms confirmed CVSM. Age/breed/sex/type of performance/degree of neurological deficits and number/sites/quality/therapy of stenosis were recorded. Sixty‐two horses met the inclusion criteria. The majority of the horses were aged 5–10 years (44%) or >10 years (35%); nine horses (15%) were 1–4 years and four <1 year (6%) old. Forty‐six horses were Warmbloods (73%), 10 ponies (16%) and six of other breeds (11%). Males were more affected (69%) than females (31%). Sixty‐one percent were pleasure‐horses, 26% were sport‐horses and no information was available for 13%. Most cases presented with mild–moderate neurological signs (grade 2/5 = 18%, grade 2–3/5 = 31%). On myelograms, 23 horses (37%) had single‐level, 22 (35%) had double‐level, and eight (13%) triple‐level stenosis, while nine cases (15%) did not have stenosis. Fifty horses (55%) showed dynamic and 41 (45%) static stenosis. Dynamic stenosis was more common (46%) than static (29%) stenosis and/or combined stenosis (25%). Stenoses were more frequently observed in the mid‐to‐caudal vertebrae. Static stenoses tended to be located more caudally. Based on our protocol, 15% of horses were subjected to euthanasia without therapy, 62% treated conservatively and 23% underwent cervical ventral interbody fusion. In conclusion, our diagnostic work‐up protocol provided practical reference points for in vivo diagnosis/prognosis and adequate management of CVSM in a nonracing horse population.     

Evaluation of poor performance in competition horses: A musculoskeletal perspective. Part 1: Clinical assessment

Lack of willingness to go forward freely, lack of power, shortened steps, stiffness of the cervical or thoracolumbosacral regions are common nonspecific signs of musculoskeletal causes of poor performance in sports horses. Understanding musculoskeletal causes of poor performance requires knowledge of how normal horses move, the requirements of specific work disciplines, the nomenclature used by riders to describe how a horse is performing and the interactions between horses and riders. Determining the underlying causes needs an in‐depth history and clinical assessment, including in hand, on the lunge and ridden. Ridden exercise should include all aspects with which the rider is experiencing problems. Change of the rider can sometimes help to differentiate between horse and rider problems, but most normal horses are compliant and just because a horse goes better for a more skilled rider does not preclude an underlying pain‐related condition. Lungeing and ridden exercise should include not only trot but also transitions and canter which may highlight gait abnormalities not seen at trot. An accurate history combined with thorough clinical examination of the whole horse should permit the establishment of a list of problems requiring further investigation.     

Equine laminitis: Induced by 48 h hyperinsulinaemia in Standardbred horses

Reasons for performing study: Hyperinsulinaemia is known to induce laminitis experimentally in healthy ponies with no history of the condition. Horses are more insulin sensitive than ponies and whether prolonged hyperinsulinaemia and euglycaemia would have a similar laminitogenic effect requires study. Objectives: To determine if laminitis results when the prolonged euglycaemic hyperinsulinaemic clamp technique (p‐EHC) is applied to clinically normal Standardbred horses, and to monitor hoof wall temperature seeking an association between vascular activity and laminitis development. Methods: Eight young, clinically normal Standardbred horses were assigned into 4 pairs and within each pair, one was assigned randomly to either treatment (n = 4) or control (n = 4) groups. Treated horses received continuous infusions of insulin and glucose until clinical signs of laminitis developed, at which point the horses were subjected to euthanasia. Control horses received an equivalent volume of a balanced electrolyte infusion for the same period. Hoof wall surface temperature (HWST) was monitored continuously throughout the experimental period. Results: All horses in the treatment group were calculated to have normal insulin sensitivity. All treated horses, and none in the control group, developed laminitis (P = 0.01). Pronounced digital pulses were a feature of the treatment group, while insignificant digital pulses occurred in control horses. HWST was higher and less variable in treated horses once hyperinsulinaemia was established. Conclusions: Healthy Standardbred horses subjected to prolonged hyperinsulinaemia develop laminitis within 48 h, demonstrating that laminitis in horses can be triggered by insulin. Potential relevance: Insulin resistance and the associated hyperinsulinaemia place horses and ponies at risk of developing laminitis. This study demonstrates a need for prompt management of the persistent hyperinsulinaemia seen in some endocrinopathies.