Investigating factors contributing to reduced embryo survival in farm‐raised Atlantic salmon,Salmo salar L.

Embryo mortality of Atlantic salmon, Salmo salar, has been increasing for more than a decade in the State of Maine, a leading producer of this species in the United States. Increasing embryo mortality not only creates a financial bottleneck for farms but also prevents the sale of surplus eggs as an additional source of revenue. Blood and egg samples were collected at three Maine Atlantic salmon farms from female broodstock at the time of spawning over a 2‐year period. Correlative factors for reduced embryo survival were investigated by measuring egg and maternal plasma concentrations of 17β‐estradiol (E2), 11‐ketotestosterone (11‐KT), testosterone and calcium, as well as maternal hepatic ethoxyresorufin‐O‐deethylase (EROD) activity and fork length. Significant positive correlations were found between maternal plasma concentrations of E2 and 11‐KT and embryo survival. Interestingly, there was no correlation with egg concentrations of sex steroids and embryo survival, suggesting that embryo mortality does not likely rest with the maternal deposition of sex steroids into the egg, but with another hormone regulated process related to egg assembly, ovulation or post‐ovulatory ageing.     

Resistance to <Emphasis Type="Italic">Meloidogyne chitwoodi</Emphasis> Identified in Wild Potato Species

Meloidogyne chitwoodi (Columbia root-knot nematode, CRKN) can cause serious damage in potato production systems, decreasing tuber value in the fresh market and processing industries. Genetic resistance to CRKN was first identified from the wild diploid potato species Solanum bulbocastanum accession SB22 and was successfully introgressed into tetraploid potato breeding material. To expand the base of genetic resistance, 40 plant accessions representing nine wild potato species were screened for their resistance to M. chitwoodi. Greenhouse screening identified fifteen clones from S. hougasii, one clone from S. bulbocastanum, and one clone from S. stenophyllidium with moderate to high levels of resistance against three isolates of M. chitwoodi. Geographical mapping showed that the resistance sources identified in this and previous studies primarily originated in the states of Jalisco and Michoacán in west-central Mexico. These new sources of resistance will be introgressed into elite potato populations to facilitate the development of potato cultivars with durable resistance to M. chitwoodi.     

Effects of 4 classes of cardiovascular drugs on ventricular function in dogs with mitral regurgitation

BACKGROUND: There have been few trials in which dogs with mitral regurgitation (MR) have been treated with various cardioactive drugs to determine effects on left ventricular (LV) function. HYPOTHESIS: Four classes of cardiovascular drugs may improve LV function in dogs with MR without increasing MR. ANIMALS: Nine mature dogs were included in the study. METHODS: MR was produced in 9 dogs. Five months later under butorphanol narcosis, parameters of LV function and left atrial dimension (LAD) were monitored by LV micromanometry and echocardiography/Doppler. Dogs were given (in random order) enalaprilat, nitroglycerine, ouabain, milrinone, and placebo. RESULTS: Nitroglycerin produced no significant change; milrinone and ouabain increased contractility; ouabain decreased heart rate; and there was evidence that enalaprilat and milrinone decreased LAD. Milrinone and ouabain decreased isovolumetric contraction time and therefore the time available for MR. There was no evidence that a positive inotrope increased MR despite increasing LV contractility and stroke volume. CONCLUSION AND CLINICAL IMPORTANCE: This study contradicts the hypotheses that (1) strengthening the left ventricle may increase MR and (2) treatment of MR (even before symptoms of heart failure develop) may decrease LAD. It is reasonable that strengthening the force of LV contraction should increase the driving pressure for MR; however, this effect did not appear to increase MR. Although some investigators believe that treating dogs with MR with afterload reducers and decreasing hindrance to ejection of blood from the LV to aorta may lengthen life by decreasing MR, there did not appear to be a reduction in MR, at least in response to the angiotensin-converting enzyme (ACE) inhibitor.     

Evidence for or against clinical efficacy of preload reducers

A preload reducer is any compound or maneuver that decreases end-diastolic ventricular volume. The determinants of preload and elevated preload are described in this article. Methods to lower preload and the future of preload reduction are discussed.     

Effects of acute gastric distention and recovery on tendency for ventricular arrhythmia in dogs

The gastric distention-volvulus (GDV) syndrome occurs commonly in large-breed dogs and may prove fatal in 15-68% of cases. Approximately 43% of cases with gastric distention (GD) or volvulus develop cardiac arrhythmias that can contribute to mortality. Most of these arrhythmias are ventricular in origin and ventricular fibrillation (VF) may be the cause of death. This study used an iatrogenic model of acute GD to investigate the prevalence of ventricular arrhythmias during acute GD and its recovery, if programmed electrical stimulation (PES) may uncover tendency to VF, if the Q-T interval corrected for heart rate (Q-Tc) of the electrocardiogram (ECG) predicts tendency to VF, and if hemodynamic changes predate VF. Eleven beagles, anesthetized with morphine and alpha-chloralose, and instrumented so that vascular pressures, cardiac output, and PES could be recorded, were used. Five were unperturbed, whereas acute GD to a pressure of 30 mm Hg for 1.5 hours was produced in 6 others. The results were as follows. No dogs with GD developed spontaneously occurring arrhythmias. VF was produced in no dogs by conventional PES, but occurred in all dogs (P < .05) with GD and none of the controls, using accelerated ventricular pacing. The Q-Tc interval of the ECG prolonged minimally in dogs with GD, and shortened (P < .05) in controls. Some hemodynamic changes did predate VF. In conclusion, dogs with acute GD have a tendency for VF, which may be uncovered by accelerated PES. The mechanism for the vulnerability to arrhythmia with GD is unknown.     

Cardiovascular effects of intravenous diltiazem in dogs with iatrogenic atrial fibrillation

Atrial fibrillation (AF) was induced in anesthetized Beagle hounds to determine the dose of diltiazem (D) that resulted in hemodynamic function similar to that observed during sinus rhythm (SR). Dogs were instrumented to record hemodynamic and electrophysiological parameters. Six dogs were given D, IV at cumulative doses of 0.063, 0.188, 0.438, 0.938, and 1.938 mg/kg, whereas 6 other dogs received vehicle in equivalent volumes. Plasma concentrations (PC) of D were measured. A cumulative dose of D between 0.438 and 0.938 mg/kg produced PC of 67.8 to 117.4 ng/mL and resulted in a heart rate (HR) closest to that observed during SR. At doses up to 0.938 mg/kg, no parameter of systolic function fell below that obtained during SR. At a dose of 0.938 mg/kg, the left ventricular end-diastolic and right atrial pressures exceeded those during SR. The rate-pressure product did not differ from that during SR at a dose of 0.938 mg/kg and fell below that during SR at the dose of 1.938 mg/kg. Left ventricular efficiency decreased from SR to AF, returned to values not different from those during SR at a dose of 0.938 mg/kg, and increased to values above those observed during SR at a dose of 1.938 mg/kg. In AF, slowing the HR with 0.438-0.938 mg/kg of D with resultant PC of 67.8-117.4 ng/mL results in cardiovascular function not different from that observed during SR.     

Retrospective trainer-reported incidence and predictors of health and training-related problems in standardbred racehorses

Information on the incidence of injury, illness, and unexplained loss of athletic performance of 2345 Standardbred racehorses was gathered from a telephone survey of 177 trainers during the 1996-1997 season. Trainer-reported incidence of infection and illness (18%) was higher than the incidence of musculoskeletal problems (10%) or unexplained athletic performance loss (6%). Older horses (>5 years) were more likely to develop musculoskeletal problems (odds ratio [OR] = 3.9; confidence interval [CI] = 1.8-8.2) and performance loss OR = 2.3, CI = 1.1-5.2) than 2-year-old horses. Horses were more likely to suffer musculoskeletal problems if fast-worked on tracks or surfaces with no banking compared with those fast-worked on tracks with banking similar to commercial racetracks OR = 4.6, CI = 2.0-9.9). Horses given no warm-up before high-intensity exercise were more likely to suffer a musculoskeletal problem than horses given a light warm-up of 1 to 9 minutes OR = 2.5, CI = 1.5-4.4). Horses trained for more than 164 min·wk⁻¹ were more likely to suffer musculoskeletal problems OR = 1.7, CI = 1.1-2.8) and athletic performance loss OR = 2.5, CI = 1.4-4.4) than horses trained for shorter periods. Horses given a moderate weekly exercise duration (132-148 min·wk⁻¹) had the lowest rates of infection and illness, but short (114-131 min·wk⁻¹) or very long (>164 min·wk⁻¹) weekly exercise duration increased the risk of horses suffering infection and illness OR = 1.6, CI = 1.1-2.2 and OR = 1.3, CI = 1.0-1.9, respectively). We conclude that Standardbred trainers could avoid many training and health problems by using well-banked tracks, providing a proper warm-up, and avoiding excessive training.

Introduction

Racehorses suffer from a variety of health and training problems that may result in poor performance. Musculoskeletal injury is a major problem in Thoroughbred racehorses, accounting for as much as 53% of the lost training and racing days.[1 and 2] Thoroughbreds that race too often, [2 and 3] have insufficient training before racing, [4] or perform too much high-speed work [5] have a greater risk of musculoskeletal problems. Performance may also be affected by respiratory infection, which is responsible for 12% of lost training or racing days. [1]Poor performance can also develop in an otherwise apparently healthy horse. Such unexplained loss of athletic performance may arise from undiagnosed health problems or from too much training.[6] Overtraining described as a state of prolonged fatigue caused by too much training or insufficient recovery [7] has been demonstrated in horses in both cross-sectional and longitudinal studies, [8 and 9] but the incidence of athletic performance loss because of overtraining in the population is unknown. Recently reported prospective studies that used the same group of horses has found that overtraining appeared to be difficult to induce in horses, [10, 11, 12 and 13] which may indicate that overtraining accounts for little of the loss in athletic performance suffered by Standardbred racehorses.It is thought that lameness is the most important cause of poor racing performance in Standardbreds[14]; however, the incidence of musculoskeletal problems causing lameness in Standardbreds is lacking. There is also little information on the incidence of respiratory disease or athletic performance loss in Standardbreds. The purpose of this study was to determine the trainer-reported incidence of these problems in Standardbred racehorses and to reveal any association with factors such as sex, age, ability, training, track surface, and track design.

Materials and methods

A survey was administered by telephone to 177 Standardbred racehorse trainers randomly selected from a list of 300 trainers compiled by Harness Racing New Zealand. The survey was administered at the end of the 1996-1997 racing season, which lasts from about September through June, and questions asked during the survey related to the 1996-1997 racing season. Trainers were asked to recall the total number of horses that experienced an unexplained and consistent loss of athletic performance (“performance decrease that lasted for at least two weeks, which was not obviously as a result of tying up, infection, illness, or musculoskeletal problems”). Trainers were also asked for the total number of horses that suffered infection or illness (viral and bacterial infections and respiratory diseases but not bleeding from the lungs), and musculoskeletal problems (lameness caused by muscle, tendon, bone, or back injuries that resulted in lost training days). Pilot work involved testing the questionnaire on 10 local horse trainers; from their feedback and that of other colleagues and horse trainers, more than 11 revisions were made. The interview consisted of 65 questions and lasted approximately 20 minutes. The incidences of performance loss and health problems detailed in this study are trainer-diagnosed; however, in the majority of cases (80%), the horses were also examined by a veterinarian and their diagnosis was consistent with the trainer's. Unfortunately, full details of the veterinary examination were not obtained during this study.To examine the influence of track design and banking, trainers were asked to compare the banking of their training tracks to the banking of a commercial racetrack (Forbury Park Raceway, Dunedin, New Zealand, which had a banking angle of approximately 2.3 degrees). Trainers had to decide whether the banking of their track was more, less, or about the same as the banking of the commercial track. Because of the need to keep the questionnaire to a reasonable size, in-depth training data was collected on only one particular group of horses—qualified maidens. Qualified maiden racehorses (previously raced but unplaced) represent the largest group of racehorses in training in New Zealand. Trainers were also asked whether they trained their other horses (faster, slower, unqualified, 1-7, or >7 wins) any differently from the qualified maidens. Information on training type, duration, and intensity were gathered for each day of a typical training week. Exercise duration and total training workload was divided into quintiles (5 equal sections) and contrasts between the quintiles were then examined. Trainers were specifically asked about the duration of the warm-up, which was not included in the total training time. Warm-up was defined as the initial preparatory phase of a training session in which the horse is slowly accustomed to low-intensity exercise and prepared for further high-intensity exercise.Although it is acknowledged that career wins is a crude method of assessing racing ability, it was the most appropriate method available to the researchers during a phone interview that gave some indication of horses' ability. Trainers were therefore asked about the number of wins for each horse and horses were grouped according to the total number of career wins. The Human Ethics Committee of the University of Otago reviewed and approved this project (reference number 97/049).The survey data were analyzed using a repeated-measures general modeling procedure (Proc Genmod, SAS Institute, Cary, NC), which estimated the effect of age, sex, gait, number of wins, warm-up, track design, training duration, and workload as odds ratios ORs). The OR is a way of comparing whether the probability of a certain event is the same for two groups. An OR of 1 implies that the event is equally likely in both groups, whereas an OR of more than one implies that the event is more likely in the first group compared with the second. For example, the odds of a horse suffering a musculoskeletal injury if fast-worked on tracks with no banking is 0.52 (cases/noncases = 12 injured/23 noninjured), whereas the odds of a horse suffering a musculoskeletal injury on well-banked tracks is 0.11 (37 injured/329 noninjured). Therefore, the OR is 4.6 and is interpreted as: 4.6 horses suffer a musculoskeletal injury if fast-worked on an unbanked track compared with every 1 horse that suffers the same injury when fast-worked on well-banked tracks. Proc Genmod (SAS Institute) analyzed the total number of horses in a particular subgroup and the total number of problems in the same subgroup for each trainer. A type I error of 5% was chosen for declaration of statistical significance; precision of estimates was represented by the 95% confidence interval (CI), the likely range of the true value.To estimate the reliability of the trainer's responses, a second questionnaire identical to the first was administered to 17 randomly selected trainers from the same sample 8 months after the original survey. The trainers' responses to the same questions from separate surveys given 8 months apart were used to gauge reliability of the survey. Questions on the sex, gait, and number of race wins of the horses under the trainers' care that suffered health and training-related problems were analyzed. These variables represented population characteristics of the horses that could change with time as horses entered or left the trainers stables, and therefore affect the reliability of the reported data. Survey reliability was found by comparing the empirical standard error of the odds ratio from the initial (Main) and second (Rely) surveys after adjustment for sample size. When the empirical standard error was similar (within one decimal place) between studies, then reliability was considered low, but when the empirical standard error was smaller in the Rely survey compared with the Main survey, then the reliability of the survey was acceptable.

Results

Overall training and health problems

Horses were 2.1 times more likely to suffer from infections and illness than from musculoskeletal problems (CI = 1.4-2.8, P < .001) and musculoskeletal problems were 1.7 times more likely to occur than athletic performance loss (CI = 1.2-2.3, P < .001). Horses that had no recognized problems raced 12 ± 6 times (mean ± SD) over the main racing season (September 1996-June 1997).

Athletic performance loss

Sixty-eight trainers reported that a total of 146 horses developed a decrease in athletic performance not readily associated with musculoskeletal injury, illness, or tying-up during the season (6% of the 2345 horses sampled). Most horses (78%) that suffered athletic performance loss required at least 6 weeks to recover to normal form; the remaining 22% recovered within 4 weeks. In general, the decrease in athletic performance occurred towards the middle and end of the racing season. The incidence of athletic performance loss in the various subgroups of horses is shown in Table 1, and the ORs and confidence limits for statistically significant differences in incidence within each subgroup are shown in Table 2.     

Correlation of QT dispersion with indices used to evaluate the severity of familial ventricular arrhythmias in Boxers

OBJECTIVE: To measure QT interval duration and QT dispersion in Boxers and to determine whether QT variables correlate with indices of disease severity in Boxers with familial ventricular arrhythmias, including the number of ventricular premature complexes per day, arrhythmia grade, and fractional shortening. ANIMALS: 25 Boxers were evaluated by ECG and echocardiography. PROCEDURE: The QT interval duration was measured from 12-lead ECG and corrected for heart rate (QTc), using Fridericia's formula. The QT and QTc were calculated for each lead, from which QT and QTc dispersion were determined. Echocardiography and 24-hour ambulatory ECG were performed to evaluate for familial ventricular arrhythmias. Total number of ventricular premature complexes, arrhythmia grade, and fractional shortening were determined and used as indices of disease severity. RESULTS: There was no correlation between any QT variable and total number of ventricular premature complexes, arrhythmia grade, or fractional shortening. No difference between QT dispersion and QTc dispersion was identified, and correction for heart rate did not affect the results. CONCLUSIONS AND CLINICAL RELEVANCE: QT interval duration and dispersion did not correlate with indices of disease severity for familial ventricular arrhythmias. Heart rate correction of the QT interval did not appear to be necessary for QT dispersion calculation in this group of dogs. QT dispersion does not appear to be a useful noninvasive diagnostic tool in the evaluation of familial ventricular arrhythmias of Boxers. Identification of affected individuals at risk for sudden death remains a challenge in the management of this disease.