HORSES
Alcohol and Gaming Commission of Ontario (AGCO) Equine Incidents in Ontario Racing: 2003 - 2017 postmortem summary
The Alcohol and Gaming Commission of Ontario (AGCO; formerly the Ontario Racing Commission, ORC) continues in its proactive approach to advance racehorse welfare and safety of human and animal participants. In 2003, Ontario became one of the first North American racing jurisdictions to require mandatory reporting of racehorse deaths, in order to monitor, research and improve knowledge of why these events occur. Postmortem (PM) exams conducted at the Animal Health Laboratory through the AGCO Equine Incidents program continue to provide comprehensive data regarding the causes of morbidity and mortality in racehorses in this province. To date, PM has been carried out on 1075 horses through the Equine Incidents program (Table 1). Annual variation in the number of PM cases reflects discretionary requirement for PM on the part of the Registrar of AGCO.
A summary of significant PM findings is provided in Table 2. A comprehensive review of AGCO PM cases was conducted in 2015 as part of a separate retrospective study and as a result, some cases have been reclassified from results presented in previous editions of the AHL Newsletter. Results of the study were published in the July 2017 edition of the Journal of Veterinary Diagnostic Investigation.
Since 2015, computed tomography (CT) of fractured and contralateral limbs has been carried out on select Equine Incidents postmortem cases through collaboration with the Diagnostic Imaging section of the Ontario Veterinary College Health Sciences Center. The goal of this in-depth examination is to identify pre-existent lesions, primarily in bone, that contribute to catastrophic fractures. The procedure was continued in 2017, with CT imaging of 31 of 34 (91%) limb fracture cases submitted for PM exam. Pre-existent lesions in bone were identified by CT and considered predisposing to fracture in 15 of 31 (48%) cases.
Exercise-associated sudden death is of special concern among those cases reported through the Equine Incidents program (Table 3). In 2017, the cause of death was investigated in 9 horses that died while exercising. Of these, significant pulmonary hemorrhage was evident in 6 horses, and no cause of death was identified in 3 horses. Among all sudden death cases from 2003-2017, significant pulmonary hemorrhage was identified in 84 of 172 (49%) of horses. The cause of death in such cases is often attributed to exercise-induced pulmonary hemorrhage (EIPH), although the pathogenesis of pulmonary hemorrhage in these horses is not well understood. Severe acute hemorrhage involving pericardium or body cavities was identified in 30 of 163 (18%) sudden death cases in previous years, but this finding was not present in any of the sudden death horses examined in 2017. In a significant proportion of exercise-associated sudden death cases from 2003-2017, no significant lesions were identified and the cause of death remained undetermined (40/172, 23%). It has been speculated that exercise-associated cardiac arrhythmia, leading to acute heart failure and pulmonary hypertension, may be the underlying cause of death among many of these horses, and may also contribute to pulmonary hemorrhage in these animals.
Summaries of postmortem submissions to the Animal Health Laboratory under this program and diagnoses by body system for these cases are provided in the tables on page 11. AHL
References
DeLay J. Postmortem findings in Ontario Racehorses, 2003-2015. J Vet Diagn Invest 2017;29:457-464.
Physick-Sheard PW, McGurrin MKJ. Ventricular arrhythmias during race recovery in Standardbred racehorses and associations with autonomic activity. J Vet Intern Med 2010;24:1158-1166.
Table 1. Breed distribution of AGCO Equine Incidents submissions to the AHL, 2003-2017
|
Breed / year |
Standardbred |
Thoroughbred |
Quarter Horse |
Total |
|
2003 |
63 |
59 |
0 |
122 |
|
2004 |
81 |
60 |
0 |
141 |
|
2005 |
59 |
51 |
0 |
110 |
|
2006 |
58 |
46 |
2 |
106 |
|
2007 |
66 |
53 |
3 |
122 |
|
2008 |
27 |
24 |
0 |
51 |
|
2009 |
28 |
16 |
1 |
45 |
|
2010 |
22 |
8 |
2 |
32 |
|
2011 |
24 |
18 |
4 |
46 |
|
2012 |
20 |
14 |
0 |
34 |
|
2013 |
19 |
26 |
2 |
47 |
|
2014 |
21 |
22 |
8 |
51 |
|
2015 |
29 |
24 |
3 |
56 |
|
2016 |
15 |
32 |
3 |
50 |
|
2017 |
26 |
34 |
2 |
62 |
|
Total |
558 |
487 |
30 |
1075 |
Table 2. Significant postmortem lesions identified in AGCO Equine Incidents submissions by body system, 2003-2017.
|
Diagnoses by body system |
2003 |
2004 |
2005 |
2006 |
2007 |
2008 |
2009 |
2010 |
2011 |
2012 |
2013 |
2014 |
2015 |
2016 |
2017 |
|
Fracture / limbs |
51 |
69 |
48 |
43 |
58 |
16 |
3 |
7 |
5 |
2 |
22 |
23 |
25 |
27 |
34 |
|
Fracture / other |
10 |
4 |
6 |
11 |
8 |
5 |
0 |
3 |
6 |
2 |
2 |
8 |
4 |
4 |
1 |
|
Non-fracture musculoskeletal |
8 |
7 |
8 |
7 |
5 |
4 |
4 |
2 |
0 |
0 |
2 |
3 |
4 |
1 |
6 |
|
Gastrointestinal |
16 |
22 |
17 |
16 |
18 |
4 |
4 |
6 |
5 |
6 |
4 |
6 |
5 |
5 |
5 |
|
Respiratory (including EIPH) |
17 |
12 |
5 |
4 |
11 |
6 |
15 |
7 |
9 |
7 |
4 |
6 |
4 |
3 |
6 |
|
Cardiovascular |
5 |
6 |
3 |
6 |
1 |
6 |
2 |
2 |
2 |
1 |
5 |
2 |
0 |
2 |
2 |
|
CNS |
3 |
7 |
8 |
4 |
0 |
1 |
2 |
0 |
6 |
2 |
3 |
0 |
2 |
2 |
0 |
|
Renal |
0 |
1 |
0 |
0 |
2 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
0 |
|
Other / whole body (e.g. septicemia) |
2 |
0 |
6 |
3 |
5 |
2 |
4 |
2 |
5 |
4 |
3 |
2 |
6 |
3 |
4 |
|
Injection-associated |
2 |
6 |
3 |
5 |
3 |
2 |
5 |
1 |
5 |
5 |
1 |
0 |
3 |
0 |
1 |
|
Cause of death undetermined |
8 |
7 |
6 |
7 |
11 |
5 |
6 |
2 |
3 |
5 |
1 |
1 |
3 |
3 |
3 |
|
Total |
122 |
141 |
110 |
106 |
122 |
51 |
45 |
32 |
46 |
34 |
47 |
51 |
56 |
50 |
62 |
Table 3. Significant postmortem lesions recorded in exercise-associated sudden death cases, AGCO Equine Incidents, 2003-2017.
|
Body system affected and significant lesions / cause of death |
Cases |
Total |
|
Respiratory EIPH Pulmonary hemorrhage (not classified by pathologist as EIPH) Miscellaneous |
68 16 3 |
87 |
|
Cardiovascular Body cavity or pericardial hemorrhage Aortic rupture and cardiac tamponade Miscellaneous cardiac lesions |
17 13 5 |
35 |
|
Cause of death undetermined |
|
40 |
|
Skull fracture (potentially secondary to collapse) |
|
5 |
|
Sepsis / disseminated intravascular coagulation |
|
5 |
|
Total |
|
172 |
AHL accepts EIA electronic submissions via EquusLINK
Jim Fairles
You can learn more about EquusLINK at: https://www.globalvetlink.com/products/equuslink/
Advantages of this electronic submission process include:
* Faster form completion, including immediate updating of information for correction of omissions.
* Streamlined submission to the lab, including embedded color photographs of horses rather than hand drawings.
* Electronic reporting of results, and streamlined transmission of test results to CFIA.
* All results stored for immediate retrieval and immediate use (no more mailing results).
Traditional EIA submission forms will of course still be accepted.
Note from the CFIA accredited veterinarian's manual: http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/accredited-veterinarian-s-manual/chapter-3/eng/1345233051622/1345233162747?chap=2
“42. The shipment of samples must never be entrusted to the animal owner or exporter. The accredited veterinarian must be able to maintain a chain of custody for samples shipped to the laboratories.”
After-hours drop-offs at AHL-Guelph require authorized signatures to maintain chain of custody. AHL
EMS and PPID
A. Equine metabolic syndrome testing
Kris Ruotsalo, Felipe Reggeti
Equine metabolic syndrome (EMS) has been described as a condition affecting young to middle-aged horses, commonly associated with insulin dysregulation (ID), and often with altered circulating adipokine concentrations, dyslipidemia, predisposition to laminitis and possible regional or generalized adiposity.1
Insulin dysregulation encompasses both tissue insulin resistance, and persistent or intermittent hyperinsulinemia without concurrent tissue insulin resistance. In the clinical setting, insulin status may be easily assessed by “resting” or “dynamic” testing (Fig. 1). Increased baseline serum insulin concentration in horses without access to grain for 4 hours supports hyperinsulinemia. The test has low sensitivity but high specificity; however, it is important to keep in mind that conditions other than EMS can cause hyperinsulinemia, including pituitary pars intermedia dysfunction (PPID), pregnancy, stress, illness, and high energy forage. A result within reference intervals in a horse with strong clinical signs of EMS is considered equivocal. In these cases, dynamic testing is recommended due to higher sensitivity, including the oral sugar test (for details, please see: http://sites.tufts.edu/equineendogroup).
Serum glucose concentration by itself is insensitive and influenced by many factors, thus concomitant testing for serum glucose and insulin concentrations is recommended.
Ancillary tests that may be considering in the assessment of horses with EMS include leptin, a hormone produced by adipocytes. The hormone is not specific for EMS, as it may be elevated with an increased body condition score but it may be helpful to assess internal adiposity and/or to monitor response to management. In addition, a marked increase in serum leptin values has been shown to correlate with the future development of laminitis.
As horses with EMS age, concurrent PPID may develop; however, to our knowledge, there are no currently published studies establishing a causal relationship between the 2 conditions. Because PPID may also be associated with insulin dysregulation, testing endogenous ACTH, insulin and glucose concentrations may be indicated if clinical signs are supportive. AHL
Reference
Bertin FR, de Laat MA. The diagnosis of equine insulin dysregulation. Equine Vet J 2017;49:570-576.
Figure 1. Assessment of insulin dysregulation (ID) - adapted from the Equine Endocrinology Group recommendations.
B. Pituitary pars intermedia dysfunction (PPID) testing
Kris Ruotsalo, Felipe Reggeti
Pituitary pars intermedia dysfunction (PPID; “Cushing’s disease”) is an endocrine condition commonly identified in aging horses and ponies. It is considered to result from loss of dopaminergic inhibition of the pituitary gland causing excessive release of ACTH into plasma and subsequent hypercortisolemia. The diagnosis may be based on clinical signs in “full-blown” cases, but it is often more difficult in animals with subtle signs or inconclusive laboratory data.
Multiple endocrinology tests have been proposed to support a diagnosis of PPID. The 2017 Equine Endocrinology Group (http://sites.tufts.edu/equineendogroup) recommendations suggested the use of endogenous ACTH for moderate and advanced cases of PPID, and the TRH-stimulation test for equivocal or early PPID (Fig. 2). Protirelin (a synthetic analog of TRH) may be available from veterinary compounding pharmacies, however it is advisable to contact the pharmacy directly to confirm, and establish pricing.
The AHL offers a chemiluminescent ACTH test, individually and within endocrine profiles. There are no fasting requirements related to sampling, however specific sample handling requirements must be adhered to. In addition to PPID, endogenous ACTH may be increased with other illness, excitement and stress.
A “seasonal increase” in ACTH has been documented during the fall months, with median concentrations ~2 times the upper reference limit (although some healthy horses showed significantly higher values). This seasonal increase has an impact in the interpretation of laboratory results. Reference intervals at the AHL (2-10 pmol/L) were developed outside the seasonal rise; thus, as an example, an ACTH result of 18 pmol/L could be unremarkable in the fall but would be interpreted as increased for the remainder of the year. The seasonal rise in ACTH may also be exaggerated in early PPID, increasing the sensitivity of the test, however seasonally adjusted reference intervals would be required for accurate interpretation.
Further, some of the clinical and laboratory findings of PPID overlap with other endocrine conditions, such as equine metabolic syndrome, occasionally making diagnostic interpretation challenging. AHL
Figure 2. Assessment of PPID - adapted from the Equine Endocrinology Group recommendations.