Charles Ja

Risk of fatality and causes of death of Thoroughbred horses associated with racing in Victoria, Australia: 1989-2004

REASONS FOR PERFORMING STUDY Determining the risk of fatality of Thoroughbred horses while racing is essential to assess the impact of intervention measures designed to minimise such fatalities. OBJECTIVES To measure the risk of racehorse fatality in jump and flat starts on racecourses in Victoria, Australia, over a 15 year period and to determine proportional mortality rates for specific causes of death. METHODS All fatalities of Thoroughbred horses that occurred during or within 24 h of a race were identified from a database. The risk of a start resulting in a racehorse fatality in all races and within flat and jump races, proportional mortality rates, population attributable risk, population attributable fraction and risk ratios were calculated along with 95% confidence intervals. Poisson regression was also performed to estimate risk ratios. RESULTS There were 514 fatalities over the 15 year period; 316 in flat races and 198 in jump races. The risk of fatality was 0.44 per 1000 flat starts and 8.3 per 1000 jump starts (18.9 x greater). The risk of fatality on city tracks was 1.1 per 1000 starts whereas on country tracks it was 0.57 per 1000 starts. Of the 316 fatalities in flat races, 73.4% were due to limb injury, 2.5% to cranial or vertebral injury and 19.0% were sudden deaths. Of the 198 fatalities in jump races, 68.7% were due to limb injury, 16.2% to cranial or vertebral injury and 3.5% were sudden deaths. The risk of fatality in flat starts increased between 1989 and 2004 but the risk in jump starts remained unchanged over the 15 year period. CONCLUSIONS The risk of fatality in flat starts was lower in Victoria than North America and the UK but the risk in jump starts was greater. Catastrophic limb injury was the major reason for racehorse fatality in Victoria but there was a larger percentage of sudden deaths than has been reported overseas. The risk of fatality in jump starts remained constant over the study period despite jump racing reviews that recommended changes to hurdle and steeple races to improve safety. POTENTIAL RELEVANCE This study provides important benchmarks for the racing industry to monitor racetrack fatalities and evaluate intervention strategies.

Outbreak of equine herpesvirus type 1 myeloencephalitis: new insights from virus identification by PCR and the application of an EHV-1-specific antibody detection ELISA.

Five of 10 pregnant, lactating mares, each with a foal at foot, developed neurological disease. Three of them became recumbent, developed complications and were euthanased; of the two that survived, one aborted an equine herpesvirus type 1 (EHV-1)-positive fetus 68 days after the first signs were observed in the index case and the other gave birth to a healthy foal on day 283 but remained ataxic and incontinent. The diagnosis of EHV-1 myeloencephalitis was supported by postmortem findings, PCR identification of the virus and by serological tests with an EHV-1 -specific ELISA. At the time of the index case, the 10 foals all had a heavy mucopurulent nasal discharge, and PCR and the ELISA were used to detect and monitor EHV-1 infection in them. The status of EHV-1 infection in the five in-contact mares was similarly monitored. Sera from three of the affected mares, taken seven days after the index case were negative or had borderline EHv-1 -specific antibody titres. In later serum samples there was an increase in the titres of EHv-1 -specific antibody in two of the affected mares. In contrast, sera from the five unaffected in-contact mares were all EHv-1 -antibody positive when they were first tested seven or 13 days after the index case.

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.

Use of transcolonic portal scintigraphy to evaluate efficacy of cellophane banding of congenital extrahepatic portosystemic shunts in 16 dogs

OBJECTIVE To evaluate the efficacy of cellophane banding of single congenital extrahepatic portosystemic shunts in dogs using transcolonic portal scintigraphy. To investigate the portal circulation of those dogs with elevated postoperative shunt fractions to determine the cause of the persistent shunting. Further, to evaluate whether presenting signs, clinical pathology findings and liver histopathology are predictive of outcome. DESIGN Prospective study of 16 dogs presenting with single congenital extrahepatic portosystemic shunts. PROCEDURE Dogs with single extrahepatic portosystemic shunts attenuated by cellophane banding underwent portal scintigraphy and bile acids tolerance testing pre- and post-operatively. Dogs identified with elevated shunt fractions at 10 weeks post-operatively underwent mesenteric portovenography. Qualitative hepatic histopathology from all dogs was reviewed by a veterinary pathologist and assigned a semi-quantitative score to identify any abnormalities that may predict surgical outcome. RESULTS At 10 weeks post cellophane banding, 10 of 16 cases (63%) had normal shunt fractions, whilst six dogs (37%) had increased shunt fractions and seven dogs (44%) had increased serum bile acids. Of these dogs, mesenteric portovenography revealed incomplete closure of the shunt in three dogs (18.6%) and multiple acquired shunts in three dogs (18.6%). Liver histopathology findings were similar for all dogs, regardless of outcome. CONCLUSIONS Cellophane banding is an efficacious method for complete gradual occlusion of single extrahepatic shunts when the shunt vessel is attenuated to < or = 3 mm. Transcolonic portal scintigraphy is a reliable method for assessment of shunt attenuation and, unlike serum bile acids, is not influenced by other causes of liver dysfunction.

Cerebral Cryptococcal Granuloma in a Cat

A 7-year-old cat was presented for seizures. Cerebrospinal fluid cytology and serology were consistent with a diagnosis of toxoplasmosis. The cat was treated with clindamycin but seizures continued and additional neurological signs developed over 6 months. A mass lesion was identified in the left cerebral hemisphere using magnetic resonance imaging (MRI). The lesion enhanced after gadolidium and a tumour was considered likely. Histologically, the lesion proved to be a cryptococcal granuloma and retrospective serology confirmed that the cat had cryptococcosis at its initial presentation. This report provides the first description in the veterinary literature of the MRI appearance of a cerebral cryptococcoma and emphasises the importance of performing cryptococcal antigen determination in cats with signs of intracranial disease.

Uropathogenic virulence factor FimH facilitates binding of uteropathogenic Escherichia coli to canine endometrium

Pyometra is a potentially life-threatening condition in bitches and is often caused by Escherichia coli infection. Both pathogenic and non-pathogenic E. coli strains commonly carry the genes for type 1 fimbriae that mediate bacterial adhesion onto host epithelium. To investigate whether the type 1 fimbrial adhesin, FimH, facilitates the binding of uropathogenic E. coli to canine endometrium, the fimH gene was insertionally inactivated in a pathogenic E. coli strain. The ability of E. coli to bind to canine endometrial epithelial cells was determined in vitro using canine uterine biopsies. Binding of the fimH mutant was only 0.3% of that of the wild type. Complementation of the mutation restored the phenotype to that of the parent. This study has developed an in vitro model that allows quantitative and qualitative assessment of bacterial binding to canine endometrium and has demonstrated that the fimH gene plays a role in adherence of pathogenic E. coli to canine endometrium.

The role of Type 1, P and S fimbriae in binding of Escherichia coli to the canine endometrium

Escherichia coli (E. coli) is the most commonly isolated infectious agent causing pyometra in bitches. Many E. coli strains isolated from the uteri of infected dogs carry several adhesin genes (fimH, papGIII and sfa). The objective of this study was to investigate the role of each adhesin gene product, acting alone or expressed in combination, in the bacterial binding to canine endometrium. E. coli strain P3, which was isolated from a uterus of a bitch naturally affected with pyometra, was shown by PCR to carry all three known fimbrial adhesin genes fimH, papGIII and sfa. Knockout (KO) mutants of this wildtype (P3-wt) strain were generated using insertional inactivation. Adhesion assays on anoestrous uteri of three post-pubertal bitches were undertaken. Overall, the number of bacteria adhering to canine endometrial biopsies was comparable between strains and no significant difference in the number of bound bacteria was found between the P3-wt strain and the single or double KO-strains. However, the triple knockout strain displayed less binding to the canine endometrium compared with the P3-wt strain. This study shows that a pathogenic E. coli strain (P3) isolated from the uterus of a bitch with pyometra was able to fully compensate for the loss of two of its three known adhesin genes. It was necessary to inactivate all three known adhesin genes in order to see a significant decrease in binding to canine endometrium.

Double-outlet right ventricle in a 10-month-old Friesian filly

A 10-month-old Friesian filly had a presentation that was consistent with chronic left- and right-sided congestive heart failure. Clinical pathology findings included abnormal haematological and biochemical variables, abnormal blood gas values and increased serum concentration of cardiac troponin I. Echocardiography revealed cardiac chamber dilation and dextropositioning of the aorta. Radiography revealed a generally enlarged heart and pulmonary interstitial infiltration. These findings were supported at necropsy and the diagnosis of double-outlet right ventricle was confirmed. The pathological changes and physiological responses subsequent to double-outlet right ventricle have not previously been described in detail in horses. Clinical progression closely resembles that seen in humans, in whom antemortem diagnosis relies on echocardiography. In horses, complex cardiac disease presents a diagnostic challenge to the clinician. Appropriate therapy must be based on an accurate diagnosis.

Cerebral cryptococcal granuloma in a cat: pp. 201-206

In the December issue of Journal of Feline Medicine and Surgery, the following case report was published with several errors. The corrected version of this case report follows in full. The publishers apologise for this error. A 7-year-old spayed domestic shorthaired cat presented with a history of having two seizures in the previous 6 weeks. During the seizures, the cat lost consciousness, paddled its limbs, rolled and urinated. There were no pre-ictal signs but the cat was weak and unable to walk normally in the post-ictal period.

In vitro evaluation of canine leukocytes radiolabeled in whole blood with 99mTc stannous colloid

INTRODUCTION Technetium-99m stannous colloid ((99m)TcSnC)-labeled leukocytes are used to investigate a variety of inflammatory diseases in human medicine. The present study investigates the in vitro behavior of canine leukocytes labeled in whole blood with (99m)TcSnC. METHODS Blood samples from 10 healthy dogs were labeled with (99m)TcSnC using a standard procedure. The distribution of radioactivity among blood components (plasma, leukocyte layers and erythrocytes) was measured following separation of the radiolabeled samples across Histopaque density gradients. Phagocytic function of labeled and unlabeled leukocytes was estimated using zymosan particles. Labeling retention by leukocytes was determined at 1, 3, 4 and 7 h postlabeling. RESULTS The mean+/-standard error percentage of radioactivity associated with plasma, erythrocyte and leukocyte fractions was 2.0+/-0.21%, 55.5+/-0.60% and 42.5+/-0.54%, respectively (the last comprising 70.2+/-0.83% in polymorphonuclear leukocytes and 29.8+/-0.83% in mononuclear leukocytes). Labeled canine leukocytes had a phagocytic activity of 91.3+/-0.28% (control, 91.7+/-0.26%). The radiolabeled canine leukocytes retained 94.1+/-0.30% of radioactivity at 7 h postlabeling. CONCLUSIONS Radiolabeling of canine leukocytes in whole blood with (99m)TcSnC has minor adverse effect on their phagocytic function. The radiolabeled canine leukocytes retained a large percentage of radioactivity for at least 7 h postlabeling.