Auscultation and echocardiographic findings in Bull Terriers with and without polycystic kidney disease.

OBJECTIVE: To investigate a possible association between Bull Terrier polycystic kidney disease (BTPKD) and cardiac disease, to determine the prevalence of mitral valve disease (MVD) and left ventricular outflow tract obstruction (LVOTO) in the Australian Bull Terrier population, and to compare auscultation and echocardiography in detection of cardiac disease in Bull Terriers. DESIGN: Ninety-nine Bull Terriers, ranging in age from 8 weeks to 13 years and 11 months were auscultated and examined using renal ultrasonography; 86 were also examined using echocardiography. The prevalence and severity of heart defects in dogs with BTPKD was compared with that in dogs without BTPKD. RESULTS: Nineteen of these 99 dogs were diagnosed with BTPKD. Forty-two percent of Bull Terriers with BTPKD and 28% of those without BTPKD had murmurs characteristic of mitral regurgitation or LVOTO. How recently an animal was descended from an ancestor with BTPKD was associated with presence (P = 0.008) and loudness of a murmur (P = 0.009). Overall, echocardiography detected MVD in 39% of Bull Terriers, with increased prevalence in older animals (P = 0.003). Mitral stenosis was found in eight cases. Fifty-three percent of dogs in this study had evidence of LVOTO, with obstruction consisting of a complex of lesions including dynamic or fixed subvalvular LVOTO, significantly narrowed left ventricular outflow tract or valvular aortic stenosis. Dogs with BTPKD, or those descended from dogs with BTPKD, were more likely to have MVD (P = 0.006), and while LVOTO was not more common in these dogs, if they did have LVOTO, they were more likely to have severe obstruction than dogs with no ancestors with BTPKD (analysed in three ways P = 0.028 to 0.001). In this study, 46% of Bull Terriers without a murmur or arrhythmia had cardiac disease detected on echocardiographic examination. CONCLUSION: Cardiac disease, especially MVD and LVOTO, was common in Bull Terriers in this study, and those with BTPKD had an increased risk of cardiac abnormalities. Auscultation did not detect a significant number of Bull Terriers with cardiac disease.

Echocardiographic parameters in 14 healthy English Bull Terriers.

OBJECTIVE: To determine the range of various cardiac parameters using echocardiography in apparently normal, healthy English Bull Terriers. DESIGN: Fourteen English Bull Terriers were selected for study. Cardiac auscultation of the parents of these dogs was normal. Echocardiographic examination of one parent of each animal showed: no mitral or aortic valve abnormalities; no myocardial lesions; no two dimensional evidence of fixed or dynamic left ventricular outflow tract obstruction; and no systolic aortic or left ventricular outflow tract turbulence on colour flow Doppler examination. The 14 selected dogs did not have arrhythmias or murmurs, and on echocardiographic examination had similar findings to their parents. Systolic blood pressure was measured in all dogs and they had no clinical evidence of Bull Terrier polycystic kidney disease or Bull Terrier hereditary nephritis. PROCEDURE: All dogs were auscultated and subjected to a sequential global echocardiographic assessment of the heart, including two dimensional long and short axis, and colour flow Doppler interrogation of the mitral and aortic valves. Dimensional measurements, including those from the left atrium, aortic annulus and left ventricle, were taken from a right parasternal window, and derived values such as fractional shortening, stroke volume and left atrial to aortic annulus ratio were calculated. Peak systolic aortic velocity was measured from the left parasternal window using two dimensional-guided pulsed wave Doppler with angle correction. Systolic blood pressure was measured using a Doppler monitor. The absence of Bull Terrier polycystic kidney disease was determined using renal ultrasonography, and of Bull Terrier hereditary nephritis using urinary protein to creatinine ratio. RESULTS: These 14 dogs had greater left ventricular wall thickness and smaller aortic root diameters than those reported as normal for other breeds of comparable body size. Left atrial dimensions were also larger, however this may have been due to the "maximising" method of measurement. These apparently normal English Bull Terriers also had higher aortic velocities than those reported for other breeds, possibly due to a smaller aortic root diameter or other anatomic substrate of the left ventricular outflow tract, lower systemic vascular resistance, or breed-specific "normal" left ventricular hypertrophy. While these dogs were selected to be as close to normal as possible, the breed may have a particular anatomy that produces abnormal left ventricular echocardiographic parameters. CONCLUSION: These echocardiographic parameters may be used to diagnose left ventricular outflow tract obstruction and left ventricular hypertrophy, and inaccurate diagnoses may result if breed-specific values are not used.

The spread of transgene expression at the site of gene construct injection.

Seven 2-day-old golden retriever pups were given focal intramuscular injections of a first generation adenovirus-dystrophin minigene construct and adenovirus-beta-galactosidase construct as a 2:1 mixture into the left anterior tibial muscle. The spread of transgene expression within the anterior tibial muscle was compared with the spread of methylene blue dye after identical injection into the contralateral muscle. Transgene expression 5-7 days after intramuscular injection was shown to extend between 5.8 and 11.6 mm along the biopsied muscle length (range of biopsy lengths 11.1-12.2 mm). The level of transgene expression at 2-2.5-mm intervals from the site of injection was significantly related to the distance from the site of injection (dystrophin, P = 0.009; beta-galactosidase, P = 0.015). The spread of methylene blue dye within the anterior tibial muscle < or =24 h after identical intramuscular injection demonstrated a similar pattern to the transgene expression, with dye staining measured between 5.5 and 8.5 mm along the muscle sample length (range of biopsy lengths 5.6-15.6 mm). The greatest transgene expression and dye staining was measured 2-2.5 mm proximal to the site of injection with a maximum of 23% of muscle fibers expressing the dystrophin transgene, 95.2% expressing the beta-galactosidase transgene, and 98% of the tissue section stained with methylene blue dye. These results suggest transgene expression after focal intramuscular injection is relatively localized around the site of injection. Further research is required to develop techniques that will provide transgene expression throughout the length and breadth of a muscle.

Antibiotic prophylaxis of lower respiratory tract contamination in horses confined with head elevation for 24 or 48 hours.

OBJECTIVE: To evaluate the administration of procaine penicillin prior to or during confinement with head elevation as a means of reducing the associated accumulation of inflammatory lower respiratory tract secretions and increased numbers of bacteria within the lower respiratory tract of confined horses. DESIGN AND PROCEDURE: Two experiments were conducted to evaluate the efficacy of different dose rates and dosing frequencies. In experiment A a single low dose (15,000 IU/kg) of procaine penicillin was administered to four horses immediately prior to confinement with head elevation for 48 hours. The systemic leucocyte response, gross and cytologic characteristics of transtracheal aspirate and bacterial numbers in lower respiratory tract samples were compared with corresponding samples from two horses confined with heads elevated but not given penicillin. The efficacy of higher dose rates (20,000 IU/kg and 40,000 IU/kg) given before and during confinement with heads elevated for 24 hours was evaluated in experiment B. RESULTS: Treatment with procaine penicillin had no effect on the systemic leucocyte response or on the accumulation of inflammatory lower respiratory tract secretions at any of the dosing schedules evaluated. The number of bacteria isolated from trans-tracheal samples was reduced at 12 hours for treated horses in experiment A and at 24 hours for experiment B. beta-haemolytic Streptococcus spp were not isolated from treated horses in either experiment. Bacterial species isolated from treated horses were predominantly Pasteurella and/or Actinobacillus spp, however, members of the family Enterobacteriaceae and a Staphylococcus sp were isolated from treated horses. One treated horse in experiment A developed clinically apparent pulmonary disease. CONCLUSIONS: The prophylactic administration of penicillin before or during confinement did not reliably reduce bacterial numbers or prevent the accumulation of purulent lower respiratory tract secretions in horses confined with their heads elevated. Numbers of beta-haemolytic Streptococcus spp were reduced following treatment, suggesting that the repeated administration of procaine penicillin may have some merit as part of a strategy to prevent transport-associated respiratory disease. However, methods directed at minimising the duration of confinement with head elevation, augmentation of the clearance of accumulated secretions and prompt identification of animals in which airway inflammation has extended to the pulmonary parenchyma remain the best ways of minimising transport-associated respiratory disease.