Aortic valvular dysplasia in a calf.

Aortic valvular dysplasia, a congenital abnormality not previously reported in cattle, was diagnosed in a calf with a pulsating mass at the base of its neck, an enlarged area of cardiac dullness and a loud (grade IV/V) systolic cardiac murmur. Electrocardiography and thoracic radiography demonstrated that the left atrium and ventricle were enlarged. Dysplasia of two aortic valve cusps and post stenotic dilatation of the ascending aorta were identified by echocardiography and confirmed post mortem.     

Idiopathic, aseptic, effusive, fibrinous, nonconstrictive pericarditis with tamponade in a standardbred filly.

A Standardbred filly was admitted for evaluation of pleuritis and pneumonia. Heart rate was 80 to 120 beats/min, and the pulse was barely palpable. Thoracic and abdominal ultrasonography and echocardiography revealed substantial pericardial effusion with cardiac tamponade, fibrinous pericarditis, pleural effusion, and ascites. Initial electrocardiography revealed normal sinus rhythm with decreased amplitude of the QRS complexes consistent with pericardial effusion. Following thoracentesis, echocardiogram-guided pericardiocentesis was performed. Bacterial culture yielded no growth from any of the fluids, and bacteria were not seen on cytologic examination. Initial treatment included broad-spectrum antibiotic treatments, IV fluid therapy, and anti-inflammatory agent administration. On the basis of negative culture results, an immune-mediated cause was considered, and dexamethasone was instituted in a decreasing dosage regimen. Pericardial effusion, ventral edema, and ascites began to resolve within 3 days after beginning dexamethasone treatment. Thirty days following discharge, the filly was reexamined, and at that time, the prognosis for athletic performance was considered good so the horse was returned to race training. The final diagnosis in this case was idiopathic, effusive, nonconstrictive pericarditis with tamponade. Early identification, clinical understanding, and application of knowledge of the pathophysiologic mechanisms of pericarditis in horses, combined with use of diagnostic aids such as ultrasonography and aggressive therapy consisting of effusion drainage, pericardial lavage, antibiotics that penetrate the pericardium, and corticosteroids when indicated are critical for a successful outcome in horses with pericarditis.     

Phylogenetic characterisation of bluetongue viruses from naturally-infected insects, cattle and sheep in Australia

SUMMARY The polymerase chain reaction was used to detect the presence of blue-tongue virus (BTV) in a number of clinical and insect samples collected in the Northern Territory of Australia. Sequence analyses of the amplified BTV genes differentiated endemic Australian and exotic viruses. Two potential exotic BTV were detected as a result of PCR analyses of blood from sentinel animals and of the insect vector, Culicoides wadai. The detection of BTV in C wadai was the first direct demonstration of the presence of BTV in this potential vector. This new technology can significantly reduce the time taken for a diagnosis from a clinical sample and increase the amount of useful information obtained on a BTV isolate by using rapid sequencing techniques. Sequence data were used to differentiate between BTV20 isolated in 1975 and two isolates of the same serotype, isolated in 1992, and indicated that the latter were probably a recent incursion into Australia from Indonesia due to their greater VP3 sequence homology to the BTV9 (Java) than to Australian BTV isolates.     

Current research and theories on the pathogenesis of acute laminitis in the horse

A large number of studies have been undertaken in recent years aimed at furthering our understanding of the complex mechanisms underlying the common and debilitating condition of acute laminitis in the horse. Many of these studies have either reinforced or cast doubt on previously held theories on the pathogenesis of this disease, while others have suggested new mechanisms which may play a key role in its development. This review seeks to put the current hypotheses into the context of this recent body of evidence. While a unifying theory may not yet seem to be achievable, this review demonstrates that most of the current theories are not mutually exclusive. Studies utilising in vitro and in vivo models of the disease, particularly addressing the areas of inflammation, haemodynamic disturbances and enzyme activation in the hoof, as well as the preceding events occurring in the hindgut, have helped to explain many clinical observations of the disease and may possibly lead to more effective therapies and means of prevention in the future.