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Accumulating evidence indicates intense exercise can be associated with myocardial damage. Investigating the impact of maximal effort on myocardium and exploring possible association of injury with rhythm disturbance requires a high-sensitivity cardiac troponin assay. The objectives of this study were: (1) to determine the effect of racing on serum cardiac troponin I (cTnI) in Standardbred horses using a high-sensitivity assay; (2) to determine the 99th percentile of cTnI in healthy horses and investigate the effect of demographic variables on cTnI prevailing pre-race in Standardbred horses using a validated high-sensitivity assay and a contemporary assay, and; (3) to explore associations between exercise-associated arrhythmia and cTnI concentration.Racehorses (n = 145).≤ 2 h pre-race, cTnI concentrations were measured in 158 race starts. Electrocardiogram (ECG) monitoring was applied during racing and race recovery and screened for complex ventricular arrhythmia. Associations between cTnI prevailing before racing concentration, age, sex, and gait were investigated. Demographic and performance variables were evaluated for associations with cTnI concentration post-race and rhythm disturbance.Incidence of arrhythmia was 11.6% (16 horses). A significant increase in median (interquartile range) cTnI concentration of 1.36 (0.49-2.81) ng/L was found post-race (p 0.0001). Serum cardiac troponin I (cTnI) concentration prevailing pre-race was positively associated with increasing age, and gait. Serum cardiac troponin I prevailing post-race was positively associated with concentration prevailing pre-race. Interaction between arrhythmia and finishing distanced revealed horses finishing distanced and experiencing arrhythmia displayed higher cTnI release than with the presence of either alone.Racing increased cTnI concentration. Horses finishing distanced and also exhibiting arrhythmia may be experiencing myocardial compromise.

There are currently no studies detailing cardiac troponin I (cTnI) release in normal horses post-exercise using an analytically validated assay. These data are essential for selecting appropriate sampling times in equine athletes with suspected myocardial injury.To plot the magnitude and time course of cTnI release after maximal effort, using validated cTnI assays.Descriptive longitudinal study.Five clinically normal Standardbred racehorses in race training were included in the study. Horses were exercised in harness at near-race intensity. Blood samples were taken immediately pre- and post-exercise and then hourly for 24 h. Samples were analysed using the validated high-sensitivity cTnI assay and a contemporary sensitivity cTnI assay.Mean resting cTnI was 1.33 ± 0.6 s.d. ng/L (range, 0.82-2.33 ng/L) using assay A. All horses were below the detection limit at rest using assay B. Peak elevation occurred 2-6 h post-exercise with both assays (mean, 4.6 ± 1.7 and 4.0 ± 2 h, respectively). Mean peak increase in cTnI was 11.96 ± 9.41 ng/L (range, 1.72-23.76 ng/L) using assay A. Peak concentrations were detectable in three of the horses using assay B and were between 0.039 and 0.051 μg/L (mean: 0.043 ± 0.006 μg/L). All horses returned to baseline within 24 h.A small (n = 5) convenience sample was used as random sampling was not logistically possible.All horses experienced an increase in cTnI post-exercise, with peak occurring 2-6 h post-exercise. Cardiac troponin I elevation was detected earlier using the high-sensitivity assay, which may convey a diagnostic advantage. Targeted studies are needed to determine the significance of these increases.

Summary In 2000, troponin assays were adopted as the test of choice for detection of myocardial injury in man. This decision was made after extensive testing and followed a 60 year search for a biomarker of myocardial damage with sufficient analytical sensitivity and specificity. This has led to proliferation of assays for use in human medicine, each requiring extensive testing and validation before it could be made available on the open market for human use. The search for ever-more analytically sensitive assays and for a standard reference material continues. The adoption of troponin testing in veterinary medicine followed shortly after its development for use in man, providing a much-needed means of detecting and monitoring myocardial damage in horses. However, application of these tests in veterinary medicine has exclusively involved use of assays designed for and clinically validated in human patients. There is no mandated requirement for test validation in veterinary medicine and, while many of these assays have been shown to be capable of detecting equine troponin, the wide diversity of available tests, lack of validation, absence of protocols for their use and lack of standardisation make their application problematic. The objective of this review article is to address this issue, offering guidance where data are available and encouraging caution where there are none. Ultimately, the overall goal of this review is to examine critically the use of troponin assays in the horse and to promote the accurate and appropriate interpretation of valid results.

Reasons for performing study There are currently no studies detailing cardiac troponin I (cTnI) release and clearance in normal horses post exercise using an analytically validated assay. These data are essential for selecting appropriate sampling times in equine athletes with suspected myocardial damage. Objective To plot the magnitude and time course of cTnI release and clearance, using a validated cTnI assay, after maximal effort. Study design Descriptive longitudinal study. Methods Five clinically normal Standardbred racehorses in full race training were included in the study. Physical examinations were performed on subjects and blood samples were taken via jugular venipuncture pre-exercise. Horses were exercised in harness at race intensity in groups on a training track. A second blood sample was taken immediately post exercise and an intravenous catheter was then placed in a jugular vein. Hourly blood samples were taken for 24 h. All samples were collected in red top serum Vacutainer® tubes and allowed to clot for 30 min before being centrifuged and serum harvested. Serum samples were stored at −80°C until analysis. All samples were analysed using the Abbott ARCHITECT STAT High Sensitivity cTnI® assay. Results Mean resting cTnI level was 1.33 ± 0.6 ng/l (range, 0.82–2.33 ng/l). All horses exhibited an increase in cTnI level after exercise with peak elevation occurring 2–6 h post exercise (mean, 4.6 ± 1.7 h). Mean peak increase in cTnI level was 11.96 ± 9.41 ng/l (range, 1.72–23.76 ng/l). All horses returned to baseline levels within 24 h. Conclusions All horses experienced an increase in cTnI post exercise, with the peak occurring 2–6 h post exercise. Further studies are needed to determine the significance of these increases. Ethical animal research: The study protocol was approved by the University's Animal Care Committee. Explicit informed consent was obtained in writing for all client-owned animals. Source of funding: Equine Guelph. Competing interests: Dr Kavsak has received grants/honoraria/consultant/advisor fees from Abbott Laboratories, Abbott Point of Care, Beckman Coulter, Ortho Clinical Diagnostics, Randox Laboratories, Roche Diagnostics, and the Canadian Agency for Drugs and Technologies in Health. He is listed as an inventor on patents filed by McMaster University related to laboratory testing in acute cardiac care. No funding was received from the manufacturer of the assay evaluated in this study.

In 2000, troponin assays were adopted as the test of choice for detection of myocardial injury in man. This decision was made after extensive testing and followed a 60 year search for a biomarker of myocardial damage with sufficient analytical sensitivity and specificity. This has led to proliferation of assays for use in human medicine, each requiring extensive testing and validation before it could be made available on the open market for human use. The search for ever-more analytically sensitive assays and for a standard reference material continues. The adoption of troponin testing in veterinary medicine followed shortly after its development for use in man, providing a much-needed means of detecting and monitoring myocardial damage in horses. However, application of these tests in veterinary medicine has exclusively involved use of assays designed for and clinically validated in human patients. There is no mandated requirement for test validation in veterinary medicine and, while many of these assays have been shown to be capable of detecting equine troponin, the wide diversity of available tests, lack of validation, absence of protocols for their use and lack of standardisation make their application problematic. The objective of this review article is to address this issue, offering guidance where data are available and encouraging caution where there are none. Ultimately, the overall goal of this review is to examine critically the use of troponin assays in the horse and to promote the accurate and appropriate interpretation of valid results.

Therapeutic renal transplantation in dogs is currently being investigated as a treatment for endstage renal disease. This pilot study examines the effect of donor bone marrow (DBM) infusion and antithymocyte serum (ATS) in combination with immunosuppressive drug therapy in prolonging renal allograft survival in dogs. Seven normal outbred mongrel dogs received an unmatched renal allograft. All dogs received rabbit anti-dog thymocyte serum (RADTS), prednisone (Pr), cyclosporine-A (CsA) and azathioprine (Aza). In addition, three dogs (group 1 test) received DBM and four dogs (group 2 control) did not receive DBM. Serum CsA levels were measured throughout the study. Immunosuppressive therapy was gradually reduced with Pr, CsA, and Aza withdrawn at 200, 450, and 680 days, respectively. Allograft rejection was treated with prednisolone sodium succinate. One dog in group 1 and one in group 2 died as a result of infectious canine rhinotracheitis and rejection early in the study. Renal allograft torsion occurred in one group 1 dog. The remaining four dogs survived the 2 years of the study. The dogs in group 2 (three dogs) all rejected the renal allograft after total drug withdrawal, the surviving dog in group 1 did not. This study demonstrates that RADTS, Pr, CsA, and Aza in combination can prolong renal allograft survival in mongrel dogs, whereas DBM may enhance the unresponsive state.

The pedigree of a line of Samoyed dogs with Samoyed hereditary glomerulopathy (SHG) was investigated to determine the mode of inheritance. Sixty percent of males were affected with severe renal disease that progressed to renal failure before 15 months of age. In contrast, female carriers showed less severe involvement and their disease did not progress to renal failure. This pattern is consistent with the inheritance of an X-linked dominant gene. A similar mode of inheritance has been postulated in some families with hereditary nephritis. Further similarities between SHG in dogs and hereditary nephritis in humans have been demonstrated previously in clinical and renal morphologic studies. The present study supports the view that this line of Samoyed dogs would be an appropriate model for studying the human disease.

The necropsy records of dairy cows with mastitis were reviewed from the provincial veterinary laboratory in Guelph (44 cases of mastitis in nine years) and from the Ontario Veterinary College (168 cases in 14 years). Mastitis was considered to be the primary cause of death in 167 of 212 cows (79%). Of these 167 cases of mastitis, Escherichia coli was involved in 107 (64%), Klebsiella sp. in 12 (7%) and Staphylococcus aureus in 11 (7%). Bacteriology was not reported in 22 cases. Coliform mastitis, the most commonly identified type of fatal mastitis, was characterized histologically by the presence of infarcted areas in affected glands and by the lack of demonstrable bacteria, and was thus easily identified from fatal mastitis caused by S. aureus.

Twenty-five steers were infected with T. vivax (EATRO 1721), 25 steers with T. congolense (EATRO 1800) and 25 steers kept as controls. Serum levels of immunoglobulins (IgG1, IgG2, IgM), natural antibodies to erythrocytes of chicken and sheep, and complement-fixing antibodies to T. vivax were measured. A significant decrease of serum IgM and natural antibodies to chicken erythrocytes occurred in the T. vivax group at day 9, i.e. at the decline of the first parasitemic wave. This was followed by a transient moderate increase of IgM accompanied by a transient decrease of IgG2. The T. congolense group had moderate decreases (less than 30%) of the mean IgG1 levels and moderate increases (less than or equal to 50%) of the mean IgG2, levels. It was concluded that there was little evidence for polyclonal activation of lymphocytes and that the decreased IgG1 levels in the T. congolense group might have been a reflection of immunosuppression. The complement-fixation test proved to be a sensitive tool for monitoring the antibody response to T. vivax.

The clearance of (51)Cr-labelled Pseudomonas endotoxin from the blood was studied in calves in a nontolerant and in an endotoxin-tolerant state. Calves were rendered tolerant to the toxic effects of the endotoxin by four daily intravenous injections of endotoxin at the dose rate of 5 microg/kg body weight. Clearance of a small amount of (51)Cr-endotoxin from the blood of nontolerant calves was almost complete within three minutes of injection and was not significantly faster in tolerant calves. The lungs and liver were the major organs involved in clearance of endotoxin from the blood. The (51)Cr label was slowly excreted by the kidneys. Neither platelets nor leukocytes were demonstrated to participate in endotoxin clearance in calves. (51)CrCl(3) was injected into control calves. Relative to the distribution and loss of labelled endotoxin, the (51)CrCl(3) was cleared slowly from the blood, was distributed uniformly throughout the body and was excreted rapidly.

Valvular competency of the foramen ovale (patent foramen ovale) is regarded as a common finding in the neonatal foal and usually occurs in isolation. True atrial septal defects appear to be uncommon and are usually associated with other congenital cardiac lesions. The present report describes a case of atrial septal defect type 1 (persistent ostium primum) complicated by hypoplastic right ventricle, and tricuspid dysplasia, in a Welsh Mountain pony foal, and discusses the embryogenesis of the abnormality. A critical review of the literature suggests that atrial septal defects may occur more frequently than they are reported, and that on occasion they may be described erroneously as patent foramen ovale. The clinical significance of uncomplicated discontinuity of the atrial septum is slight, depending upon the size and location of the defect. Complicated atrial septal defects vary in clinical significance according to the nature of the associated defects.

Strain Y3343 isolated from a goat with septicemia and polyarthritis was studied. The strain was virulent and induced septicemia, polyarthritis and coagulopathy in two goats. Limulus amebocyte lysate active material was present in plasma, but not in higher titre in inoculated goats. Sonicated mycoplasma material induced a dramatic somatic cell response in the mammary gland of cows and goats and marked clotting of the cows' milk, but it did not clot limulus amebocyte lysate or kill chick embryos. Phenol-water extract clotted limulus amebocyte lysate and induced somatic cell response in cows but not in goats. The phenol-water extract did not kill chick embryos, was not pyrogenic in rabbits or goats, and did not induce generalized Shwartzman reaction or change the leukocyte kinetics in rabbits. It therfore appears that the virulence mechanisms of strain Y3343 can not be explained on the basis of factors with strong endotoxin activity.

Four control calves were aerosolized with parainfluenza-3 and one week later with Pasteurella haemolytica. Three calves were given Corynebacterium parvum at a dose of 15 mg/m2 body surface area, infected with parainfluenza-3 virus one week later, and aerosolized with P. haemolytica two weeks after C. parvum injection. All calves were killed four hours after P. haemolytica exposure and the bacterial retention in the lung was determined. Parainfluenza-3 viral infection did not exert any suppressive effect on pulmonary clearance of P. haemolytica in six out of seven calves used. However, the bacterial colony counts in the lungs of control calves were higher (P less than 0.05) than those in calves given C. parvum. Hence, C. parvum appeared to enhance bacterial clearance. Despite the marked influx of neutrophils into the lungs after the bacterial inoculation, the neutrophil:macrophage ratio in lavage samples was less in calves given C. parvum than in the control calves. The alveolar macrophages in C. parvum treated calves were generally larger but did not differ significantly (P less than 0.05) from those in the controls. There was no significant (P less than 0.05) correlation between the percentages of alveolar macrophages and the bacterial clearance. In calves given C. parvum, bacterial clearance was enhanced in those calves which had larger macrophages.

Mammary glands of 6 lactating Holstein cows were inoculated with Haemophilus somnus strain 43826. Three cows developed chronic mastitis and shed bacteria for up to 1 year. Three cows developed acute gangrenous mastitis, with evidence of bacteremia and endotoxemia. Cows with gangrenous mastitis had lower somatic cell counts early after inoculation in affected quarter secretions compared with those in cows that developed chronic mastitis. Cows with gangrenous mastitis developed hypocalcemia, hypoalbuminemia, azotemia, hyperbilirubinemia, mildly increased serum aspartate aminotransferase and creatine kinase activity, and a marked neutropenia with a degenerative left shift. Histopathologic examination of gangrenous quarters revealed edema, necrosis, and vascular thrombosis with few inflammatory cells. A limited survey failed to recover H somnus from dairy cows with clinical mastitis or from mammary secretions from 41 beef cattle at an abattoir.

Serum collected from cattle infected with Trypanosoma vivax or Trypanosoma congolense inhibited bovine granulocyte/macrophage colony formation in methyl cellulose cultures. Maximum inhibition was caused by serum collected two and three weeks post infection. The degree of inhibition appeared to be related to the degree of parasitemia. Inhibition of erythroid colony formation by serum collected from these animals was not observed.

Twenty-five Holstein-Friesian steers were experimentally infected with Trypanosoma congolense EATRO 1721. They were tested for their J blood group status. Twelve steers were found to belong to Ja blood group and thirteen steers were either Js or Jcs. The level of parasitemia did not significantly differ between these two groups of cattle. It was concluded that the level of parasitemia is not influenced by J blood group antigens.

Marrow aspirates from calves injected with Pseudomonas aeruginosa endotoxin showed an increased number of granulocyte/macrophage progenitor cells, and a reduced number of erythroid progenitor cells. On the other hand, marrow aspirates from calves made anaemic by repeated phlebotomy showed an increased number of erythroid progenitor cells, and a reduced number of granulocyte/macrophage progenitor cells. These observations were interpreted as evidence of stem cell erythroid-granuloid directional competition occurring in response to the need for a particular cell type.

Bovine macrophage colonies were grown in liquid medium. Serum collected from a heifer 3 hours after injection of Pseudomonas aeruginosa endotoxin promoted the growth of macrophage colonies. The optimum concentration of postendotoxin serum was 16%. The numbers of colonies increased exponentially between 3 and 6 days of incubation and leveled off at 6 days. Monoblasts, promonocytes, and macrophages were observed in these colonies. A direct linear relationship between the number of nucleated bone marrow cells cultured and the number of colonies formed was found. The macrophage colony cells were positive for nonspecific esterase activity and were negative for chloroacetate esterase activity. Weak peroxidase activity was noticed in monoblasts, promonocytes, and occasionally in macrophages.

Twenty five cattle were infected with T. vivax, 25 with T. congolense, and 25 served as controls. Pathogenic clinical signs of trypanosomal infection were not observed. Secondary bacterial infections were common. Fever, increased heart and respiratory rates, anorexia, and emaciation developed. Elevations in parasitemai and body temperature were positively correlated in the T. vivax group. Infected groups were affected non-uniformly, with some animals in each group remaining asymptomatic and tending to have lower parasitemias. The T. vivax parasitemia was cyclic and the organisms had a genaration time of 7.9 SD 2.5 hours. The first peak of parasitemia in both infections was closely associated with the development of pancytopenia, i.e. anemia, leukopenia, and thrombocytopenia. The bone marrow erythroid response in the T. congolense group was significantly greater thn that in either the T. vivax or control groups. Leukopenia was due to concomitant neutropenia and lymphopenia.

Bovine erythrocytic colonies containing up to 300 cells each were produced by using a plasma clot technique with five percent CO2 at 37 degrees C. with high humidity and 2.5 units of sheep step III erythropoietin per milliliter. Erythropoietin was essential for colony formation. The number of colonies ranged from 24 to 823 per 10(5) nucleated marrow cells plated, in different animals. Some of the erythroid colonies were mixed with granulocytes. Granulocyte/macrophage colonies were produced in methyl cellulose cultures. Colonies contained up to 1000 cells and the number of colonies ranged from 13 to 981 per 10(5) nucleated marrow cells plated, from different animals. Glass adherent cells appeared to produce colony stimulating activity in culture. In both culture systems, there was a direct linear relationship between the number of nucleated marrow cells plated and the number of colonies produced.

Serum levels of total protein, albumin, activity of hemolytic complement, and complement component C3 were decreased in cattle infected with either T. congolense or T. vivax. The hemolytic complement activity was reduced most, i.e. to 20% (T. congolense) or 5% (T. vivax) of control levels. The development of hypocomplementemia was closely associated with the first peak of parasitemia.

Samoyed hereditary glomerulopathy (SHG) in dogs resembles hereditary nephritis (HN) in man. Affected males and carrier females spontaneously develop proteinuria, but only males progress to renal failure. We examined the evolution of splitting of glomerular capillary basement membranes (GCBM) in affected male and carrier female dogs. At birth, examination by light microscopy (LM) in all dogs showed normal glomerular capillaries, but by electron microscopy (EM), many GCBM showed separation of endothelial from visceral epithelial cell basement membranes. By LM, glomerular capillaries of affected males appeared normal for up to 4 months, but then isolated and eventually all capillaries became thickened and split. However, by EM, a bilaminar appearance of the GCBM was seen within 1 month which evolved into multilaminar splitting that became extensive as renal failure ensued. Carrier females showed mild nonprogressive changes in GCBM. These results with SHG permitted speculation on the evolution of splitting of GCBM in human HN.