Sudden death of a crossbred calf associated with a myocardial adenomatoid tumour.

The only lesion found in a crossbred calf that died suddenly was a rare tumour in the myocardium of the left ventricle. The mass appeared similar to tumours discovered incidentally in the hearts of abattoir specimens in Italy, described as adenomatoid tumours. These are bimorphic tumours presumed to have a mesothelial origin. Although in a published study from Italy these tumours were considered incidental and clinically unimportant, I suggest that in this case the mass may have interfered with cardiac conduction, causing sudden death of the calf.

Prevalence and risk factors for medical events following exercise at Australian Greyhound race meetings.

AIM: A prospective, observational study to determine the prevalence of post-exercise conditions at Australian Greyhound race meetings and to assess association with race performance and other environmental, race- and dog-related factors was undertaken. METHODS: A total of 4020 starters were observed (2813 Greyhounds, 1009 trainers, 536 races, 52 race meets, 48 race dates and 11 race tracks) following a race. The presence of diaphragmatic flutter (DF), ataxia, seizure, collapse or sudden death was recorded. Risk factors were screened by univariable logistic regression prior to multivariable backward stepwise model building. RESULTS: In this study, 962 starters (n = 768 dogs) had DF (23.9%), 16 starters were ataxic (0.4%) and there were no observed cases of collapse, seizure or sudden death. Race track location, increasing race distance, race grade based on increasing 1st place prize value, lower (earlier) race number at the meeting, age, a previous observation of DF at the last start, females, colour (white) and better finishing position were all associated with an increased risk of a Greyhound being observed with DF. However, when logistic regression assessing the random effect of dog was performed, the presence of previous DF was not significant. In this cohort, DF was common following strenuous exercise in Greyhounds and on its own does not appear to result in reduced performance or distress to the animal. CONCLUSION: The incidence of ataxia was low and collapse, seizure and sudden death were not observed. However, even though uncommon, ataxia has welfare concerns for racing Greyhounds that warrants further investigation.

Metastatic mineralisation caused by vitamin D intoxication in hand-raised short-beaked echidnas (Tachyglossus aculeatus).

CASE REPORT: Two cases of metastatic mineralisation caused by dietary excess of vitamin D are reported in hand-raised short-beaked echidna (Tachyglossus aculeatus) puggles at the Australian Wildlife Health Centre. Oversupplementation was attributed to excessive levels of vitamin D in Wombaroo Echidna Milk Replacer fed to the puggles. No information exists regarding the naturally occurring vitamin D levels in echidna milk, but, given the low serum levels that have been observed in free-ranging animals, it is likely to be low. CONCLUSION: The vitamin D concentration in Wombaroo Echidna Milk Replacer has been reduced.

Plasmodium infection in a Leadbeater's possum (Gymnobelideus leadbeateri).

CASE REPORT: A wild-caught, adult female Leadbeater's possum (Gymnobelideus leadbeateri) died while in captivity after suffering from chronic ill-thrift that progressed to acute respiratory distress. On histopathological examination of tissues, the cause of death was determined to be severe acute pneumonia with pulmonary oedema associated with an intracellular protozoan parasite present within erythrocytes. Transmission electron microscopy was performed on lung tissues and organisms consistent for Plasmodium sp. were identified within numerous erythrocytes. Molecular characterisation of the parasite from DNA extracted from tissue blocks of fixed lung determined the organism to belong to the genus Plasmodium (100% similarity to Plasmodium species when a BLAST analysis was performed); however, speciation of the organism was not possible. CONCLUSION: This is the first report of Plasmodium sp. infection and subsequent disease in a native Australian mammal. The lifecycle of this parasite remains unknown. It is also unknown what effects haemoparasitism may have on the population dynamics of this endangered possum species.

Encephalitozoon hellem Infection in a Captive Juvenile Freshwater Crocodile (Crocodylus johnstoni).

Microsporidiosis is reported rarely in reptiles and has never been reported in any species of crocodilian. Microsporidiosis was diagnosed histologically in a juvenile captive freshwater crocodile (Crocodylus johnstoni) that was found suddenly dead in its enclosure. Ultrastructural and molecular testing revealed infection to be due to Encephalitozoon hellem. This is the first report of E. hellem infection in any species of reptile.

Avian pox in crimson rosellas (Platycercus elegans) in southern Australia.

Poxviral infection was identified in a crimson rosella presented to the Australian Wildlife Health Centre (Victoria) in 2002, and from a second crimson rosella in 2008. Both cases were characterized by proliferative lesions on non-feathered skin. Routine histopathology identified intra-lesional epidermal changes consistent with those caused by poxvirus. Electron microscopy confirmed the presence of poxvirus in inclusions in the first case, and genetic analysis of DNA extracted from both cases found an identical viral genome that differs from all other known poxviruses. We conclude that this infection in crimson rosellas is caused by a previously unrecognized avian poxvirus endemic to this region of Australia, and with low virulence.

Murray Valley encephalomyelitis in a horse.

A 5-year-old Thoroughbred mare presented with signs of severe pain and was taken to exploratory laparotomy based on suspicion of an acute abdominal lesion. A mild gastrointestinal lesion was discovered, but was considered disproportional to the severity of signs displayed. The mare was later euthanased because of intractable pain. Comprehensive postmortem examination, including polymerase chain reaction testing of central nervous system tissue samples, allowed a definitive diagnosis of Murray Valley encephalomyelitis to be made. This case demonstrates the variability of clinical presentations in horses infected with Murray Valley encephalitis virus.

Effects of acute exercise on angiotensin I-converting enzyme (ACE) activity in horses.

Angiotensin I-converting enzyme (ACE) level measurement in blood samples is an important tool in human medicine for the detection, treatment and control of diseases such as sarcoidosis and hypertension. Recently ACE has been advocated as being correlated to athletic aptitude in human athletes and a genetic polymorphism has been shown to be responsible for the enzymatic levels in the circulation. The objective of this research was to evaluate the effects of acute exercise in horses in order to increase the understanding of a possible correlation between ACE levels in plasma and performance in equine athletes. A standardised exercise test (SET) to fatigue was conducted on 8 horses and repeated venous blood collections carried out for ACE activity measurements before, during and after the SET. Our results show an increase in ACE activity up to fatigue and a return to baseline values at 30 min post exercise.

Association between circulating angiotensin-converting enzyme and exercise-induced pulmonary haemorrhage in Thoroughbred racehorses.

Exercise-induced pulmonary haemorrhage has an impact on racehorse performance. Although endoscopic diagnosis (with or without the aid of bronchoalveolar lavage) is considered to be the standard diagnostic method for this condition, the use of biomarkers that could aid in quantifying risk and severity of the condition would represent an advance in equine sport medicine. This preliminary research investigated the use of angiotensin-converting enzyme (ACE) activity in plasma of racehorses and demonstrated that ACE activity is increased in horses with higher degrees of haemorrhage and is a promising biomarker for EIPH in racehorses.

Effects of two training protocols on Angiotensin I-converting enzyme (ACE) activity in horses.

REASONS FOR PERFORMING STUDY: Studies in man have shown a correlation between Angiotensin I-converting enzyme (ACE) genetic polymorphisms, ACE activity in the blood and superior athletic performance in sports requiring endurance. It has been hypothesised that the same correlation occurs in horses. There is no information in the literature concerning the effects of training on ACE activity in equine plasma. HYPOTHESIS: Exercise training influences the activity of circulating ACE and the response observed is dependent on the exercise protocol. METHODS: Thirteen horses of mixed breeds were randomly allocated 2 different training protocols to be carried out for a period of 15 weeks. Blood samples were collected from each horse before the beginning of training to determine baseline values. Subsequent sampling took place every 15 days throughout the training phase and for 8 weeks of paddock rest. Angiotensin I-converting enzyme activity was determined by automated spectrophotometry. RESULTS: Training for 15 weeks significantly increased plasma ACE activity, irrespective of training protocol. Differences observed in ACE activity pattern between the 2 training protocols were not statistically significant. Increase in ACE activity peaked with maximum workload. As soon as training was interrupted, ACE levels significantly decreased. CONCLUSIONS AND DISCUSSION: Exercise training affects levels of ACE activity in equine plasma. The mechanism for this is not yet elucidated, but cardiovascular adaptation to exercise and blood pressure changes might be involved in this regulation. POTENTIAL RELEVANCE: Exercise training produced a gradual increase in enzymatic activity and might warrant the use of ACE as a tool for fitness monitoring. Angiotensin I-converting enzyme enzymatic activity in the plasma might be directly correlated to a change in genetic expression and that variability must be taken into account when evaluating results from horses undergoing a physical training programme.

Sudden death in racing Thoroughbred horses: an international multicentre study of post mortem findings.

REASONS FOR PERFORMING STUDY: To improve the understanding of exercise related sudden death in Thoroughbred racehorses. OBJECTIVES: To describe the post mortem findings in cases of sudden death associated with exercise in 268 Thoroughbred racehorses. METHODS: Gross and histological post mortem findings of 268 cases of sudden death were collated and reviewed. Cases originated from 6 racing jurisdictions around the world. Sudden death was defined as acute collapse and death in a closely observed and previously apparently healthy Thoroughbred racehorse, during, or within one hour after, exercise. Cause of death as determined by the attending pathologist was categorised as definitive, presumptive or unexplained and compared between the different populations. Cardiopulmonary lesions recorded at post mortem examination were compared between different populations. RESULTS: Pathologists recorded a definitive cause of death in 53% (143/268) of cases. Major definitive causes of sudden death included cardiac failure, apparent pulmonary failure, pulmonary haemorrhage, haemorrhage associated with pelvic fractures or with idiopathic blood vessel rupture, and spinal cord injury. A presumptive cause of death was made in 25% (67/268) of cases and death remained unexplained in 22% (58/268) of cases. There were several statistically significant inter-population differences in the cause of death and in reporting of cardiopulmonary lesions. CONCLUSIONS: Sudden death can be attributed to a variety of causes. Causes of sudden death and the lesions found in cases of exercise-related sudden death are similar in different racing jurisdictions. However, the lesions are often not specific for the cause of death and determination of the cause of death is therefore affected by interpretation by the individual pathologist.

Circulating angiotensin converting enzyme in endurance horses: effect of exercise on blood levels and its value in predicting performance.

REASONS FOR PERFORMING STUDY: Investigate angiotensin converting enzyme (ACE) activity in equine plasma as a predictor of performance in endurance competitions and the effect of endurance exercise on ACE activity. HYPOTHESIS: Precompetition values of ACE activity in equine blood are correlated with performance results and with heart rates pre- and post competition used as indicators of fitness. Endurance exercise increases ACE activity. METHODS: Nineteen horses participating in an 80 km endurance competition had venous blood samples collected before and after the ride. ACE activity and total protein were measured in the blood samples and heart rates and finishing positions were recorded. Statistical analysis included paired t tests and Spearman's rank correlation coefficient. RESULTS: Of the 19 horses enlisted, only 16 horses completed the ride. Of these 16, another 2 were disqualified at the last veterinary check. When the 16 horses were considered, precompetition heart rate, but not ACE, was correlated with finishing position. When only the 14 horses that were classified were considered, the association disappeared. ACE activity was similar before and after competition. CONCLUSIONS: Precompetition ACE activity in endurance horses competing in an 80 km event was not associated with either finishing position or heart rates before or after competition, indicating that the enzyme is not a good predictor of performance in this form of equestrian competition. Endurance competition did not significantly alter ACE activity in this group of horses.

Risk factors for exercise-induced pulmonary haemorrhage in Thoroughbred racehorses.

REASONS FOR PERFORMING STUDY: Risk factors for occult exercise-induced pulmonary haemorrhage (EIPH) are poorly defined or quantified. OBJECTIVES: To investigate the importance of putative risk factors for EIPH amongst Thoroughbred racehorses in Australia. METHODS: Tracheobronchoscopy was used to determine EIPH status of 744 Thoroughbred racehorses after flat racing in Melbourne, Australia. Horses were identified for study before racing, and over 50% of horses racing during the study period were examined. Statistical analysis included use of bivariate and multivariate logistic regression analysis to account for simultaneous effects of a large number of variables. RESULTS: The only risk factor identified as associated with both EIPH ≥ 1 or ≥ 2 was ambient temperature, with horses racing at temperatures <20 °C being at ∼ 2 times risk of occult EIPH. There was no association of EIPH with age, sex, weight carried, track hardness, speed of racing, or air quality. CONCLUSIONS: There do not appear to be individual risk factors, amongst those examined in this study, that are strongly associated with EIPH. POTENTIAL RELEVANCE: The risk of developing EIPH cannot be readily determined from a combination of age, race speed, race distance, track hardness or air quality. This study does not provide support for the hypotheses that racing on hard surfaces or in polluted air contributes to the development of EIPH.

Experimental mild pulmonary inflammation promotes the development of exercise-induced pulmonary haemorrhage.

REASONS FOR PERFORMING STUDY: Histological studies of exercise-induced pulmonary haemorrhage (EIPH) reveals inflammatory infiltrates within areas of lung that contain haemorrhage. This has resulted in the hypothesis that pulmonary inflammation could cause EIPH or contribute to an increased risk or severity of EIPH. OBJECTIVES: To determine whether experimentally-induced pulmonary inflammation predisposes the lung to haemorrhage during exercise, by evaluating the bronchoalveolar lavage (BAL) cytology of normal and inflamed regions of lung following high speed treadmill exercise. MATERIALS AND METHODS: Transendoscopic airway inoculations of 0.01% acetic acid were used to induce mild localised inflammation within bronchopulmonary segments. Horses underwent high speed exercise 24 h after inoculation. Following exercise, inoculated sites and corresponding segments in the opposite lung underwent BAL. The cytology results from inflamed and control bronchopulmonary segments were compared, using paired t tests. RESULTS: Erythrocytes were present in BAL samples from 12.5% (1/8) control segments compared with 75% (6/8) inoculated segments following exercise, indicating a significant increase (P = 0.04) in the relative risk of EIPH following the development of pulmonary inflammation. Samples from inoculated segments had significantly higher percentages and numbers of neutrophils (12.1 ± 1.0% and 601 ± 98 cells/µl) than control samples (4.3 ± 0.3% and 214 ± 52 cells/µl). Significantly higher erythrocyte numbers were observed in samples from inoculated segments (14,304 ± 6862 cells/µl) compared with control samples (3.5 ± 3.5 cells/µl). CONCLUSIONS: The results showed inflammation increased the risk of developing pulmonary haemorrhage during exercise. These findings do not conflict with current theories on the common causes of EIPH, but suggest that care should be taken when recommending exercise in horses suspected to be suffering from pulmonary inflammatory disease. In addition, specific therapy to reduce pulmonary inflammation may benefit horses prone to the development of EIPH.

Auricular chondrosis in a horse.

A 4-year-old crossbred, Welsh Mountain Pony gelding was presented with multiple, thick, round, raised, 3 to 8 mm diameter nodular lesions on the medial aspects of both ears. The nodules did not involve the epidermis and were observed to develop over several months. Punch biopsies were taken and histopathological examination returned a diagnosis of auricular chondrosis. Neither auricular chondrosis nor auricular chondritis has been reported in horses, although it has been recorded in cats, dogs, laboratory animals and humans.

Lethal toxoplasmosis in an aviary of kakarikis (Cyanoramphus spp.) in Australia.

A small outbreak of fatal toxoplasmosis is described in 6 kakariki (Cyanoramphus spp.) in an aviary in Australia. Toxoplasma gondii-like tachyzoites were found associated with necrosis in intestine, spleen, liver, and lungs. Protozoal tachyzoites reacted positively with T. gondii-specific polyclonal antibodies. This is the first report of toxoplasmosis in kakariki.

Risk factors for Thoroughbred racehorse fatality in jump starts in Victoria, Australia (1989-2004).

REASONS FOR PERFORMING STUDY: The risk of fatality is greater in jump than in flat racing in Victoria, Australia. This is the first study to identify risk factors specific to jump starts in Victoria. OBJECTIVE: To identify risk factors for fatality of Thoroughbred racehorses in jump starts on all racecourses in Victoria, Australia between 1989 and 2004. METHODS: Fatalities comprised all horses that died during or immediately after a jump (hurdle or steeplechase) race or official jump trial and all horses that were subjected to euthanasia within 24 h of an event in which an injury was sustained. The retrospective study involved 191 case starts and 2324 control starts. Univariable and multivariable backward stepwise logistic regression was used to identify risk factors for fatality at any one start. A multiple level model was used with racecourse included as a random effect. RESULTS: In the final multivariable model, the duration of the racing career of the horse, the number of flat, hurdle and steeple starts accumulated in the 60 days prior to the case or control start, the number of flat and jump starts accumulated over the racing career, if the horse had had a start between 1 and 14 days prior to the case or control start, the type of jump race (hurdle or steeple), the calendar year of the start and the location of the racecourse were associated with fatality. CONCLUSIONS: The findings highlight the need to investigate further the differences between hurdle and steeplechase events and the adverse effect of prolonged prior flat racing careers on the risk of fatality in jump starts. POTENTIAL RELEVANCE: This is the first study to examine risk factors for fatality in jump starts in Victoria. The results should shape the development of interventions to reduce the risk in jump starts in the future.

Risk factors for Thoroughbred racehorse fatality in flat starts in Victoria, Australia (1989-2004).

REASONS FOR PERFORMING STUDY: Research into risk factors specific for fatality in flat racing should be focused at a regional level as the risk factors may differ among countries and even regions within countries. OBJECTIVE: To identify risk factors for fatality of Thoroughbred racehorses in flat starts on all racecourses in Victoria, Australia between 1989 and 2004. METHODS: Fatalities comprised all horses that died during or immediately after a flat race or official flat trial, and all horses that were subjected to euthanasia within 24 h of an event in which an injury was sustained. The retrospective study involved 283 case starts and 3307 control starts. Univariable and multivariable backward stepwise logistic regression was used to identify risk factors for fatality at any one start. RESULTS: In the final multivariable model, horse gender, prior racing history, race length, racing year, racecourse location and track rating were associated with fatality. CONCLUSIONS: This study identified specific risk factors for fatality. The findings are consistent with the hypothesis that horses accumulating high speed exercise are predisposed to catastrophic injury. The study has also highlighted the need to investigate further the adverse effects of different track ratings on the incidence of injury and subsequent fatality. RELEVANCE: The results will facilitate the development of effective strategies to improve overall safety of horses and jockeys in flat racing in Victoria, Australia.

Gallbladder mucocoele and concurrent hepatic lipidosis in a cat.

A 3-year-old Domestic Shorthair cat was presented with weight loss, anorexia and icterus. Feline hepatic lipidosis and gallbladder mucocoele were diagnosed; this is the first report of gallbladder mucocoele in the cat. The case was managed successfully with cholecystojejunostomy, gastrostomy tube placement and tube feeding for 3 months. The cat has survived over the long term with minimal complications.

Pulmonary response to airway instillation of autologous blood in horses.

REASONS FOR PERFORMING STUDY: Exercise-induced pulmonary haemorrhage (EIPH) occurs in the majority of horses performing strenuous exercise. Associated pulmonary lesions include alveolar and airway wall fibrosis, which may enhance the severity of EIPH. Further work is required to understand the pulmonary response to blood in the equine airways. OBJECTIVES: To confirm that a single instillation of autologous blood into horse airways is associated with alveolar wall fibrosis, and to determine if blood in the airways is also associated with peribronchiolar fibrosis. METHODS: Paired regions of each lung were inoculated with blood or saline at 14 and 7 days, and 48, 24 and 6 h before euthanasia. Resulting lesions were described histologically and alveolar and airway wall collagen was quantified. RESULTS: The main lesion observed on histology was hypertrophy and hyperplasia of type II pneumocytes at 7 days after blood instillation. This lesion was no longer present at 14 days. There were no significant effects of lung region, treatment (saline or autologous blood instillation), nor significant treatment-time interactions in the amount of collagen in the interstitium or in the peribronchial regions. CONCLUSION: A single instillation of autologous blood in lung regions is not associated with pulmonary fibrosis. POTENTIAL RELEVANCE: Pulmonary fibrosis and lung remodelling, characteristic of EIPH, are important because these lesions may enhance the severity of bleeding during exercise. A single instillation of autologous blood in the airspaces of the lung is not associated with pulmonary fibrosis. Therefore the pulmonary fibrosis described in EIPH must have other causes, such as repetitive bleeds, or the presence of blood in the pulmonary interstitium in addition to the airspaces. Prevention of pulmonary fibrosis through therapeutic intervention requires a better understanding of these mechanisms.